Biological scaffolds have been the focus of bone tissue engineering research in recent years. In this paper, emodin (EM), macromolecular compound polycaprolactone (PCL), and hydroxyapatite (HA) were used as raw materi...Biological scaffolds have been the focus of bone tissue engineering research in recent years. In this paper, emodin (EM), macromolecular compound polycaprolactone (PCL), and hydroxyapatite (HA) were used as raw materials to prepare EM/PCL/HA fibers containing different EM ratios by electrospinning, and the properties and osteogenic efficacy of EM/PCL/HA were studied. Scanning electron microscopy, transmission electron microscopy, and atomic force microscopy were used to characterize the structures of HA and the electrospun fibers. Results showed that HA has high crystallinity and loose porous structure, and the electrospun fibers have a smooth and flat surface. In vitro release results showed that EM was slowly released from EM/PCL/HA within 216 h. Cell proliferation assay in mouse embryonic osteoblast precursor cells (MC3T3-E1) exhibited that 5% EM/PCL/HA had the best effect on promoting cell proliferation. Alkaline phosphatase (ALP) and mineralized nodules staining results also showed that 5% EM/PCL/HA had the best effect on promoting osteogenic differentiation. qRT-PCR results showed that the mRNA expression level of osteoblast differentiation markers, namely, bone morphogenetic protein (BMP)-2, BMP-9, and osteocalcin were significantly upregulated by 5% EM/PCL/HA treatment. These results indicate that EM/PCL/HA is a potential osteogenic material, which can provide a reference for the development of bone injury repair materials.展开更多
Emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous system.However,the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown.In ...Emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous system.However,the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown.In this study,a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis,and the rats were intraperitoneally injected with emodin(20 mg/kg/d)from the day of immune induction until they were sacrificed.In this model,the nucleotide-binding domain-like receptor family pyrin domain containing 3(NLRP3)inflammasome and the microglia exacerbated neuroinflammation,playing an important role in the development of multiple sclerosis.In addition,silent information regulator of transcription 1(SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator(PGC-1α)was found to inhibit activation of the NLRP3 inflammasome,and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis.Furthermore,treatment with emodin decreased body weight loss and neurobehavioral deficits,alleviated inflammatory cell infiltration and demyelination,reduced the expression of inflammatory cytokines,inhibited microglial aggregation and activation,decreased the levels of NLRP3 signaling pathway molecules,and increased the expression of SIRT1 and PGC-1α.These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis,possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation.These findings provide experimental evidence for treatment of multiple sclerosis with emodin,enlarging the scope of clinical application for emodin.展开更多
Emodin is an effective component of rhubarb with positive pharmacological effects on human health.However,it is also toxic to different cells or tissues to varying degrees.The effects of emodin on glomerular endotheli...Emodin is an effective component of rhubarb with positive pharmacological effects on human health.However,it is also toxic to different cells or tissues to varying degrees.The effects of emodin on glomerular endothelial cells(GECs)remain to be tested,and the documented works were always performed in vitro and hardly reflect the real physiological situation.To study the effects of emodin on GECs in a biomimetic environment,we utilized a microfluidic chip to assess the physiological reaction of human renal glomerular endothelial cells to various concentrations of emodin in this work.The results showed that emodin caused cytotoxicity,impaired glomerular filtration barrier integrity to macromolecules,and increased barrier permeability in a dose-dependent manner.With the increase in emodin concentration,the concentration of the pro-inflammatory cytokine tumor necrosis factor-α,interleukin(IL)-6,transforming growth factor-β1,and monocyte chemoattractant protein(MCP-1)increased while the production of inflammatory cytokine IL-6 first increased and then decreased with the increase in emodin concentration.Our findings shed new light on emodin-induced nephrotoxicity and provide insights for the application of microfluidic chip devices to reveal drug-cell interactions.展开更多
INTRODUCTIONIn order to study the therapeutic mechanisms ofemodin,an extract of Rhubarb （Rhizoma et RadixRhei,a traditional Chinese herbal medicine）,andsandostatin in the treatment of acute necrotizingpancreatitis ...INTRODUCTIONIn order to study the therapeutic mechanisms ofemodin,an extract of Rhubarb （Rhizoma et RadixRhei,a traditional Chinese herbal medicine）,andsandostatin in the treatment of acute necrotizingpancreatitis （ANP）,we used the two drugs in ratmodels of the disease and observed the changes ofplasma thromboxane-2（TXB<sub>2</sub>）,6-keto-prostaglandin F<sub>1α</sub>(6-keto-PGF<sub>1α</sub>)and prostaglandinE<sub>2</sub>（PEG<sub>2</sub>）.展开更多
BACKGROUND:Emodin,a traditional Chinese medicine,has a therapeutic effect on severe acute pancreatitis(SAP),whereas the underlying mechanism is still unclear.Studies showed that the intestinal mucosa impairment,and su...BACKGROUND:Emodin,a traditional Chinese medicine,has a therapeutic effect on severe acute pancreatitis(SAP),whereas the underlying mechanism is still unclear.Studies showed that the intestinal mucosa impairment,and subsequent release of endotoxin and proinflammatory cytokines such as IL-1β,which further leads to the dysfunction of multiple organs,is the potentially lethal mechanism of SAP.Caspase-1,an IL-1β-converting enzyme,plays an important role in this cytokine cascade process.Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP.METHODS:Eighty Sprague-Dawley rats were randomly divided into four groups(n=20 each group):SAP,sham-operated(SO),emodin-treated(EM) and caspase-1 inhibitor-treated(ICE-I) groups.SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct.Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction.Serum levels of IL-1β,IL-18 and endotoxin,histopathological alteration of pancreas tissues,intestinal mucosa,and the intestinal caspase-1 m RNA and protein expressions were assessed 24 hours after SAP induction.RESULTS:Rats in the SAP group had higher serum levels of IL-1β and IL-18(P<0.05),pancreatic and gut pathological scores(P<0.05),and caspase-1 m RNA and protein expressions(P<0.05) compared with the SO group.Compared with the SAP group,rats in the EM and ICE-I groups had lower IL-1β and IL-18 levels(P<0.05),lower pancreatic and gut pathological scores(P<0.05),and decreased expression of intestine caspase-1 m RNA(P<0.05).Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions,more disappeared intercellular joints,and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups.CONCLUSIONS:Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP.Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines,including IL-1β and IL-18.Our animal data may be applicable in clinical practice.展开更多
AIM: To investigate the effect of emodin on expression of claudin4, claudin5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate. METHODS: Experimental pan...AIM: To investigate the effect of emodin on expression of claudin4, claudin5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate. METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Emodin was injected via the external jugular vein 3 h after induction of acute pancreatitis. Rats from sham operation group and acute pancreatitis group were injected with normal saline (an equivalent volume as emodin) at the same time point. Samples of lung and serum were obtained 6 h after drug administration. Pulmonary morphology was examined with HE staining. Pulmonary edema was estimated by measuring water content in lung tissue samples. Tumor necrosis factorα (TNFα) and interleukin6 (IL6) level were measured by enzymelinked immunospecific assay. Serum amylase and pulmonary myeloperoxidase (MPO) activity were detected by spectrophotometry. Alveolar epithelial barrier was assessed by pulmonary dye extravasation. Expression of claudin4, claudin5 and occludin in lung tissue samples was examined by immunohistology, quantitative realtime reverse transcription polymerase chain reaction and Western blotting analysis, respectively.RESULTS: Pancreatitis-associated lung injury was char-acterized by pulmonary edema, leukocyte infiltration, alveolar collapse, and elevated serum amylase level. The pulmonary damage, pulmonary pathological scores, serum amylase and MPO activity, TNF-α and IL-6 levels, and wet/dry ratio were decreased in rats after treatment with emodin. Immunostaining of claudin-4, claudin-5 and occludin was detected in lung tissue samples from rats in sham operation group, which was distributed in alveolar epithelium, vascular endothelium, and bron-chial epithelium, respectively. The mRNA and protein expression levels of claudin-4, claudin-5 and occludin in lung tissue samples were markedly decreased, the expression level of claudin-4, claudin-5 and occluding was increased, and the pulmonary dye extravasation was reduced in lung tissue samples from rats with acute pancreatitis after treatment with emodin.CONCLUSION: Emodin attenuates pulmonary edema and inflammation, enhances alveolar epithelial barrier function, and promotes expression of claudin-4, claudin-5 and occludin in lung tissue samples from rats with acute pancreatitis.展开更多
Objective: To study the effect of emodin on protein and gene expressions of the massagers in mobility signal transduction system of cholecyst smooth muscle cells in guinea pig with cholesterol calculus. Methods: The g...Objective: To study the effect of emodin on protein and gene expressions of the massagers in mobility signal transduction system of cholecyst smooth muscle cells in guinea pig with cholesterol calculus. Methods: The guinea pigs were randomly divided into 4 groups, such as control group, gall-stone(GS) group, emodin group and ursodesoxycholic acid(UA) group. Cholesterol calculus models were induced in guinea pigs of GS, emodin and UA groups of induced models by lithogenic diet, while emodin or UA were given to the corresponding group for 7 weeks. The histomorphological and ultrastructure change of gallbladder were detected by microscope and electron microscope, the content of plasma cholecystokinin(CCK) and [Ca^(2+)]i were analyzed successively by radioimmunoassay and flow cytometry. The protein and mR NA of Gsα, Giα and Cap in cholecyst cells were determined by western blotting and real time polymerase chain reaction(RT-PCR). Results: Emodin or UA can relieve pathogenic changes in epithelial cells and muscle cells in gallbladder of guinea pig with cholesterol calculus by microscope and transmission electron microscope. In the cholecyst cells of GS group, CCK levels in plasma and [Ca^(2+)]i decreased, the protein and m RNA of GS group were downregulated,the protein and m RNA of Gi and Cap were up-regulated. Emodin significantly decreased the formative rate of gallstone, improved the pathogenic change in epithelial cells and muscle cells, increased CCK levels in plasma and [Ca^(2+)]i in cholecyst cells, enhanced the protein and mR NA of Gs in cholecyst cells, reduced the protein and mR NA of Gi and Cap in cholecyst cells in guinea pig with cholesterol calculus. Conclusion: The dysfunction of gallbladder contraction gives rise to the disorders of mobility signal transduction system in cholecyst smooth muscle cells, including low content of plasma CCK and [Ca^(2+)]i in cholecyst cells, abnormal protein and mRNA of Gs, Gi and Cap. Emodin can enhance the contractibility of gallbladder and alleviate cholestasis by regulating plasma CCK levels, [Ca2+]i in cholecyst cells and the protein and mR NA of Gs, Gi and Cap.展开更多
AIM To investigate the effects of combined use of emodin and baicalein(CEB) at the cellular and organism levelsin severe acute pancreatitis(SAP) and explore the underlying mechanism.METHODS SAP was induced by retrogra...AIM To investigate the effects of combined use of emodin and baicalein(CEB) at the cellular and organism levelsin severe acute pancreatitis(SAP) and explore the underlying mechanism.METHODS SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha(TNf-α), interleukin 6(IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol(1,4,5)-trisphosphate receptor(IP3 R) expression were investigated to assess the mechanism of CEB.RESULTS Pancreatic histopathology score(2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity(2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB(three doses) treatment group compared with the SAP group(2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6(466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α(108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10(200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca2+ concentration, and significantly ameliorated intracellular vacuoles and IP3 m RNA expression compared with those in the SAP group(P < 0.05). There was a trend towards decreased IP3 R protein in the CEB treatment group; however, it did not reach statistical significance(P > 0.05).CONCLUSION These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.展开更多
AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cel...AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cells, the inhibition rate (IR), 50% inhibitory concentration (IC 50 ) and reversal index (IC 50 in experimental group/IC 50 in control group) were calculated. For HepG2, HepG2/OXA, HepG2/OXA/T, each cell line was divided into a control group, OXA group, OXA + fibroblast growth factor 7 (FGF7) group and OXA + emodin group, and the final concentrations of FGF7, emodin and OXA in each group were 5 ng/mL, 10 μg/mL and 10 μmol/L, respectively. Single-cell gel electrophoresis was conducted to detect DNA damage, and the fibroblast growth factor receptor 2 (FGFR2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and excision repair cross-complementing gene 1 (ERCC1) protein expression levels in each group were examined by Western blotting. RESULTS: Compared with the IC50 of 120.78 μmol/L in HepG2/OXA cells, the IC 50 decreased to 39.65 μmol/L after treatment with 10 μmol/L emodin; thus, the reversal index was 3.05. Compared with the control group, the tail length and Olive tail length in the OXA group, OXA + FGF7 group and OXA + emodin group were significantly increased, and the differences were statistically significant (P < 0.01). The tail length and Olive tail length were lower in the OXA + FGF7 group than in the OXA group, and this difference was also statistically significant. Compared with the OXA + FGF7 group, the tail extent, the Olive tail moment and the percentage of tail DNA were significantly increased in the OXA + emodin group, and these differences were statistically significant (P < 0.01). In comparison with its parental cell line HepG2, the HepG2/OXA cells demonstrated significantly increased FGFR2, p-ERK1/2 and ERCC1 expression levels, whereas the expression of all three molecules was significantly inhibited in HepG2/ OXA/T cells, in which FGFR2 was silenced by FGFR2 shRNA. In the examined HepG2 cells, the FGFR2, p-ERK1/2 and ERCC1 expression levels demonstrated increasing trends in the OXA group and OXA + FGF7 group. Compared with the OXA group and OXA + FGF7 group, the FGFR2, p-ERK1/2, and ERCC1 expression levels were significantly lower in the OXA + emodin group, and these differences were statistically significant. In the HepG2/OXA/T cell line that was transfected with FGFR2 shRNA, the FGFR2, p-ERK1/2 and ERCC1 expression levels were significantly inhibited, but there were no significant differences in these expression levels among the OXA, OXA + FGF7 and OXA + emodin groups. CONCLUSION: Emodin markedly reversed OXA resistance by enhancing OXA DNA damage in HepG2/OXA cells, and the molecular mechanism was related to the inhibitory effect on ERCC1 expression being mediated by the FGFR2/ERK1/2 signaling pathway.展开更多
A new series of bone affinity compounds were synthesized by linking emodin with 5-fluorouracil derivatives. Their bone affinities were established by hydroxyapative (HA) affinity experiment in vitro, and their cytosta...A new series of bone affinity compounds were synthesized by linking emodin with 5-fluorouracil derivatives. Their bone affinities were established by hydroxyapative (HA) affinity experiment in vitro, and their cytostatic effects were shown by the MTT assay.展开更多
Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into con...Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P<0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P<0.05),SOD level was significantly higher than that of model group(P<0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.展开更多
Severe acute pancreatitis accounts for 15% - 20% of acute pancreatitis and is a kind of serious systemic disease because it involves multiple organ damage and dysfunction. Emodin is the most important active ingredien...Severe acute pancreatitis accounts for 15% - 20% of acute pancreatitis and is a kind of serious systemic disease because it involves multiple organ damage and dysfunction. Emodin is the most important active ingredient of rhubarb and has been used for the treatment of severe acute pancreatitis. This review mainly summarizes the study progress of emodin in severe acute pancreatitis treatment.展开更多
Aim: To explore the emodin’s toxicity and action mechanism on the function of interstitial cells of Cajal (ICC) cultured in vitro. Methods: ICC of KM mouse was cultured in vitro. The minimum toxicity concentration an...Aim: To explore the emodin’s toxicity and action mechanism on the function of interstitial cells of Cajal (ICC) cultured in vitro. Methods: ICC of KM mouse was cultured in vitro. The minimum toxicity concentration and critical time points of emodin were investigated with Uniform Design methodology and MTT assay. The cell enzymology assay and enzyme immunoassay (EIA) were applied to observe the effect of emodin on membrane stability, cellular internal environment, energy metabolism and second messenger of ICC. Results: The minimum toxicity concentration was 0.001%, and the critical time points were 30 s, 1 min, 30 min, and 60 min. After administration of emodin, the damage on cells aggravated with time prolonging. The activity of malonaldehyde (MDA), lactate dehydrogenase (LDH), and phosphatase in the cell was raised significantly (P + and Ca2+ were increased but K+ concentration was decreased. The Na+-K+-ATPase activity was promoted but Ca2+-ATPase descended. Second messenger as IP3 and cAMP also became more active. All these changes had statistical significance (P Conclusion: Emodin had toxicity function on ICC which can lead to membrane damage, energy metabolism disorder. This mechanism could be related to electrolytes concentration disorder, inhibited activity of Na+-K+-ATPase and Ca2+-ATPase, and raised activity of IP3 and cAMP.展开更多
Hydroxymethylation of 6,8-O-dimethyl emodin was easily achieved in good yields by the modified Marschalk reaction.The influence of the amount of solvent,base and formaldehyde toward the hydroxymethylation was discusse...Hydroxymethylation of 6,8-O-dimethyl emodin was easily achieved in good yields by the modified Marschalk reaction.The influence of the amount of solvent,base and formaldehyde toward the hydroxymethylation was discussed.The results showed that a relatively dilute reaction solution facilitated the generation of the desired 2-hydromethyl product,while the thick reaction solution benefited the generation of the methylated quinizarins.展开更多
Over the past years natural products and/or their derivatives have continued to provide cancer chemotherapeutics. Glycosides derivatives of emodin are known to possess anticancer activities. An in silico study was car...Over the past years natural products and/or their derivatives have continued to provide cancer chemotherapeutics. Glycosides derivatives of emodin are known to possess anticancer activities. An in silico study was carried out to evaluate emodin derivatives as inhibitors of Arylamine N-Acetyltransferase 2, Cyclooxygenase 2 and Topoisomerase 1 enzymes, predict their pharmacokinetics and explore their bonding modes. Molecular docking study suggested that D2, D5, D6 and D9 to be potent inhibitors of NAT2, while D8 was suggested to be a potent inhibitor of TOP1. Derivatives D2, D5, D6 and D9 bind to the same pocket with different binding conformation. Pharmacokinetic study suggested that selected emodin derivatives can be potential cancer chemotherapeutic agent. Physicochemical parameters such density, balaban index, surface tension, logP and molar reflectance correlated to compounds activity. These finding provides a potential strategy towards developing NAT2 and TOP1 inhibitors.展开更多
Cancer is a disease caused by the loss of normal cell regulation and excessive proliferation. At present, there are a lot of anticancer drugs, but most of them are not ideal, with sereve side effects. Besides, during ...Cancer is a disease caused by the loss of normal cell regulation and excessive proliferation. At present, there are a lot of anticancer drugs, but most of them are not ideal, with sereve side effects. Besides, during the treatment, the patients feel very bad, and they are always in great pain. Emodin is a natural anthraquinone derivative found in a variety of herbal preparations. Many studies have shown that emodin has a significant therapeutic effect on lung cancer, liver cancer, breast cancer, and so on. After reviewing a large amount of literatures, this paper summarizes the research progresses of emodin anticancer in the past five years, in order to provide theoretical basis for further development and utilization of emodin and its metabolites.展开更多
Emodin [1,3,8-Trihydroxy-6-methylanthraquinone] has been reported to exhibit vascular anti-inflammatory properties.However,the relevant anti-inflammatory mechanisms are not well understood.The present study was design...Emodin [1,3,8-Trihydroxy-6-methylanthraquinone] has been reported to exhibit vascular anti-inflammatory properties.However,the relevant anti-inflammatory mechanisms are not well understood.The present study was design to explore the molecular target(s) of emodin展开更多
[Objectives]To establish a method for the determination of emodin in Wudajiangjun liquor,a hospital preparation.[Methods]A high-performance liquid chromatography(HPLC)method for the determination of emodin in Rhizoma ...[Objectives]To establish a method for the determination of emodin in Wudajiangjun liquor,a hospital preparation.[Methods]A high-performance liquid chromatography(HPLC)method for the determination of emodin in Rhizoma Polygontum Cuspidatum in hospital preparation Wudajiangjun liquor was established.Using HPLC method,octadecylsilane chemically bonded silica gel was used as filler for the chromatographic column[Inertsil-C 18 chromatographic column(5μm,4.6 mm×250 mm)].Methanol-0.1%phosphoric acid water(76∶24)was used as mobile phase.The flow rate was 1.0 mL/min,the column temperature was 30℃,the detection wavelength was 254 nm,and the injection volume was 10μL.[Results]The content of emodin in Wudajiangjun liquor was determined by reversed-phase high performance liquid chromatography(RP-HPLC).When the injection volume of emodin was in the range of 5.45-54.5μg/mL,there was a good linear relationship between the injection volume and the peak area.The regression equation is Y=42.952-15.068(r=0.9998),the average recovery rate is 98.23%,and RSD=1.45%.[Conclusions]A method for the determination of emodin in Wudajiangjun liquor by HPLC was established.This method can be used as a quality control method for Wudajiangjun liquor with high accuracy and good repeatability,which lays a foundation for the quality control of the medicinal liquor.展开更多
The present study explored quality control of plant drug and polyherbal formulation using HPTLC and HPLC fingerprinting.The study combined qualitative analysis of Emodin and Rhein biomarker compound in Rhei Emodi Wall...The present study explored quality control of plant drug and polyherbal formulation using HPTLC and HPLC fingerprinting.The study combined qualitative analysis of Emodin and Rhein biomarker compound in Rhei Emodi Wall.rhizome extract and polyherbal formulation extract by HPTLC method with quantitative estimation of Emodin by HPLC method,aiming to help in accurate identification of Emodin and Rhein in plant materials,polyherbal formulations.This study also checked adulteration,with the purpose of improving bio-efficacy of ayurvedic formulation.All the samples showed characteristic peaks of Emodin at same retention time as that of standard Emodin.According to the HPTLC fingerprinting results,the Rf values of Rhein reference standard at 0.42 and Emodin at 0.62 were observed in test solution of Rhei emodi Wall.rhizome extract and polyherbal formulation extract and both were found comparable.The quantitative evaluation of Emodin present in the polyherbal formulation and Rhei emodi Wall.rhizome extracts were 0.0177% and 0.3106% respectively.展开更多
AIM: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by high caloric laboratory chaw.METHODS: Non-alcoholic fatty liver model was successfully established by feeding ...AIM: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by high caloric laboratory chaw.METHODS: Non-alcoholic fatty liver model was successfully established by feeding with high caloric laboratory chaw for 12 wk. Then the model rats were randomly divided into 3 groups, namely model control group, emodin group and dietary treatment group. The rats in emodin group in othergroups were given distilled water of the same volume. The rats in model control group were fed with high caloric laboratory chaw while animals in other groups were fed with normal diet. Four weeks later, liver index (liver/body weight ratio), serum activities of liver-associated enzymes, blood lipid, fasting blood glucose, fasting plasma insulin, HOMA insulin resistance index (HOMA-IR), hepatic triglyceride content and histology features of all groups were assayed. The expression of hepatic peroxisomal proliferator activated receptor (PPAR) gamma was determined by RT-PCR.RESULTS: The body weight, liver index, serum activities of alanine aminotransferase (ALT), blood lipid, hepatic triglyceride content of model control group were significantly elevated, with moderate to severe hepatocyte steatosis.The expression of hepatic PPAR gamma mRNA was obviously reduced in model control group. Compared with model control group, the body weight, liver index, serum activities of ALT, blood lipids and hepatic triglyceride of emodin group significantly decreased and hepatic histology display was also greatly improved. Meanwhile, the expression of hepatic PPAR gamma mRNA was elevated.However, high serum activities of ALT and hyperlipidemia were persisted in dietary treatment group although liver index was decreased and liver histology was somewhat improved.CONCLUSION: It is suggested that emodin might be effective in the treatment of non-alcoholic fatty liver in rats. Its therapeutic mechanism could be associated with increasing the expression of hepatic PPAR gamma mRNA.展开更多
基金supported by Grants from the National Natural Science Foundation of China(No.81871756 and No.51672178)Innovation Fund of National Orthopaedic and Exercise Rehabilitation Clinical Medical Research Center(2021-NCRC-CXJJ-ZH-13).
文摘Biological scaffolds have been the focus of bone tissue engineering research in recent years. In this paper, emodin (EM), macromolecular compound polycaprolactone (PCL), and hydroxyapatite (HA) were used as raw materials to prepare EM/PCL/HA fibers containing different EM ratios by electrospinning, and the properties and osteogenic efficacy of EM/PCL/HA were studied. Scanning electron microscopy, transmission electron microscopy, and atomic force microscopy were used to characterize the structures of HA and the electrospun fibers. Results showed that HA has high crystallinity and loose porous structure, and the electrospun fibers have a smooth and flat surface. In vitro release results showed that EM was slowly released from EM/PCL/HA within 216 h. Cell proliferation assay in mouse embryonic osteoblast precursor cells (MC3T3-E1) exhibited that 5% EM/PCL/HA had the best effect on promoting cell proliferation. Alkaline phosphatase (ALP) and mineralized nodules staining results also showed that 5% EM/PCL/HA had the best effect on promoting osteogenic differentiation. qRT-PCR results showed that the mRNA expression level of osteoblast differentiation markers, namely, bone morphogenetic protein (BMP)-2, BMP-9, and osteocalcin were significantly upregulated by 5% EM/PCL/HA treatment. These results indicate that EM/PCL/HA is a potential osteogenic material, which can provide a reference for the development of bone injury repair materials.
基金supported by the National Natural Science Foundation of China,No.81771271Key Research and Development Program of Liaoning Province,No.2020JH2/10300047Outstanding Scientific Fund of Shengjing Hospital(all to JF).
文摘Emodin,a substance extracted from herbs such as rhubarb,has a protective effect on the central nervous system.However,the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown.In this study,a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis,and the rats were intraperitoneally injected with emodin(20 mg/kg/d)from the day of immune induction until they were sacrificed.In this model,the nucleotide-binding domain-like receptor family pyrin domain containing 3(NLRP3)inflammasome and the microglia exacerbated neuroinflammation,playing an important role in the development of multiple sclerosis.In addition,silent information regulator of transcription 1(SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator(PGC-1α)was found to inhibit activation of the NLRP3 inflammasome,and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis.Furthermore,treatment with emodin decreased body weight loss and neurobehavioral deficits,alleviated inflammatory cell infiltration and demyelination,reduced the expression of inflammatory cytokines,inhibited microglial aggregation and activation,decreased the levels of NLRP3 signaling pathway molecules,and increased the expression of SIRT1 and PGC-1α.These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis,possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation.These findings provide experimental evidence for treatment of multiple sclerosis with emodin,enlarging the scope of clinical application for emodin.
基金This work was supported by the National Key R&D Program of China(Project No.2018YFC1602103)Ministry of Science and Technology of China.
文摘Emodin is an effective component of rhubarb with positive pharmacological effects on human health.However,it is also toxic to different cells or tissues to varying degrees.The effects of emodin on glomerular endothelial cells(GECs)remain to be tested,and the documented works were always performed in vitro and hardly reflect the real physiological situation.To study the effects of emodin on GECs in a biomimetic environment,we utilized a microfluidic chip to assess the physiological reaction of human renal glomerular endothelial cells to various concentrations of emodin in this work.The results showed that emodin caused cytotoxicity,impaired glomerular filtration barrier integrity to macromolecules,and increased barrier permeability in a dose-dependent manner.With the increase in emodin concentration,the concentration of the pro-inflammatory cytokine tumor necrosis factor-α,interleukin(IL)-6,transforming growth factor-β1,and monocyte chemoattractant protein(MCP-1)increased while the production of inflammatory cytokine IL-6 first increased and then decreased with the increase in emodin concentration.Our findings shed new light on emodin-induced nephrotoxicity and provide insights for the application of microfluidic chip devices to reveal drug-cell interactions.
基金National Natural Science Foundation of China,No.35970891
文摘INTRODUCTIONIn order to study the therapeutic mechanisms ofemodin,an extract of Rhubarb （Rhizoma et RadixRhei,a traditional Chinese herbal medicine）,andsandostatin in the treatment of acute necrotizingpancreatitis （ANP）,we used the two drugs in ratmodels of the disease and observed the changes ofplasma thromboxane-2（TXB<sub>2</sub>）,6-keto-prostaglandin F<sub>1α</sub>(6-keto-PGF<sub>1α</sub>)and prostaglandinE<sub>2</sub>（PEG<sub>2</sub>）.
基金supported by grants from Zhejiang Province Traditional Chinese Medicine Scientific Research Fund(2011-ky1-001-164 and 2016ZB066)Public Welfare Projects of Ministry of Science of Zhejiang Province(20130101120016)
文摘BACKGROUND:Emodin,a traditional Chinese medicine,has a therapeutic effect on severe acute pancreatitis(SAP),whereas the underlying mechanism is still unclear.Studies showed that the intestinal mucosa impairment,and subsequent release of endotoxin and proinflammatory cytokines such as IL-1β,which further leads to the dysfunction of multiple organs,is the potentially lethal mechanism of SAP.Caspase-1,an IL-1β-converting enzyme,plays an important role in this cytokine cascade process.Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP.METHODS:Eighty Sprague-Dawley rats were randomly divided into four groups(n=20 each group):SAP,sham-operated(SO),emodin-treated(EM) and caspase-1 inhibitor-treated(ICE-I) groups.SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct.Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction.Serum levels of IL-1β,IL-18 and endotoxin,histopathological alteration of pancreas tissues,intestinal mucosa,and the intestinal caspase-1 m RNA and protein expressions were assessed 24 hours after SAP induction.RESULTS:Rats in the SAP group had higher serum levels of IL-1β and IL-18(P<0.05),pancreatic and gut pathological scores(P<0.05),and caspase-1 m RNA and protein expressions(P<0.05) compared with the SO group.Compared with the SAP group,rats in the EM and ICE-I groups had lower IL-1β and IL-18 levels(P<0.05),lower pancreatic and gut pathological scores(P<0.05),and decreased expression of intestine caspase-1 m RNA(P<0.05).Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions,more disappeared intercellular joints,and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups.CONCLUSIONS:Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP.Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines,including IL-1β and IL-18.Our animal data may be applicable in clinical practice.
基金Supported by National Natural Science Foundation of China, No. 30500688
文摘AIM: To investigate the effect of emodin on expression of claudin4, claudin5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate. METHODS: Experimental pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. Emodin was injected via the external jugular vein 3 h after induction of acute pancreatitis. Rats from sham operation group and acute pancreatitis group were injected with normal saline (an equivalent volume as emodin) at the same time point. Samples of lung and serum were obtained 6 h after drug administration. Pulmonary morphology was examined with HE staining. Pulmonary edema was estimated by measuring water content in lung tissue samples. Tumor necrosis factorα (TNFα) and interleukin6 (IL6) level were measured by enzymelinked immunospecific assay. Serum amylase and pulmonary myeloperoxidase (MPO) activity were detected by spectrophotometry. Alveolar epithelial barrier was assessed by pulmonary dye extravasation. Expression of claudin4, claudin5 and occludin in lung tissue samples was examined by immunohistology, quantitative realtime reverse transcription polymerase chain reaction and Western blotting analysis, respectively.RESULTS: Pancreatitis-associated lung injury was char-acterized by pulmonary edema, leukocyte infiltration, alveolar collapse, and elevated serum amylase level. The pulmonary damage, pulmonary pathological scores, serum amylase and MPO activity, TNF-α and IL-6 levels, and wet/dry ratio were decreased in rats after treatment with emodin. Immunostaining of claudin-4, claudin-5 and occludin was detected in lung tissue samples from rats in sham operation group, which was distributed in alveolar epithelium, vascular endothelium, and bron-chial epithelium, respectively. The mRNA and protein expression levels of claudin-4, claudin-5 and occludin in lung tissue samples were markedly decreased, the expression level of claudin-4, claudin-5 and occluding was increased, and the pulmonary dye extravasation was reduced in lung tissue samples from rats with acute pancreatitis after treatment with emodin.CONCLUSION: Emodin attenuates pulmonary edema and inflammation, enhances alveolar epithelial barrier function, and promotes expression of claudin-4, claudin-5 and occludin in lung tissue samples from rats with acute pancreatitis.
基金supported by the National Science Foundation of China(30672698)
文摘Objective: To study the effect of emodin on protein and gene expressions of the massagers in mobility signal transduction system of cholecyst smooth muscle cells in guinea pig with cholesterol calculus. Methods: The guinea pigs were randomly divided into 4 groups, such as control group, gall-stone(GS) group, emodin group and ursodesoxycholic acid(UA) group. Cholesterol calculus models were induced in guinea pigs of GS, emodin and UA groups of induced models by lithogenic diet, while emodin or UA were given to the corresponding group for 7 weeks. The histomorphological and ultrastructure change of gallbladder were detected by microscope and electron microscope, the content of plasma cholecystokinin(CCK) and [Ca^(2+)]i were analyzed successively by radioimmunoassay and flow cytometry. The protein and mR NA of Gsα, Giα and Cap in cholecyst cells were determined by western blotting and real time polymerase chain reaction(RT-PCR). Results: Emodin or UA can relieve pathogenic changes in epithelial cells and muscle cells in gallbladder of guinea pig with cholesterol calculus by microscope and transmission electron microscope. In the cholecyst cells of GS group, CCK levels in plasma and [Ca^(2+)]i decreased, the protein and m RNA of GS group were downregulated,the protein and m RNA of Gi and Cap were up-regulated. Emodin significantly decreased the formative rate of gallstone, improved the pathogenic change in epithelial cells and muscle cells, increased CCK levels in plasma and [Ca^(2+)]i in cholecyst cells, enhanced the protein and mR NA of Gs in cholecyst cells, reduced the protein and mR NA of Gi and Cap in cholecyst cells in guinea pig with cholesterol calculus. Conclusion: The dysfunction of gallbladder contraction gives rise to the disorders of mobility signal transduction system in cholecyst smooth muscle cells, including low content of plasma CCK and [Ca^(2+)]i in cholecyst cells, abnormal protein and mRNA of Gs, Gi and Cap. Emodin can enhance the contractibility of gallbladder and alleviate cholestasis by regulating plasma CCK levels, [Ca2+]i in cholecyst cells and the protein and mR NA of Gs, Gi and Cap.
基金Supported by National Natural Science Foundation of China,No.30901945Science Research Foundation of Shaanxi Administration of Traditional Chinese Medicine,No.15-ZY029Science Research Foundation of the Second Affiliated Hospital of Xi’an Jiaotong University,No.RC(XM)201602
文摘AIM To investigate the effects of combined use of emodin and baicalein(CEB) at the cellular and organism levelsin severe acute pancreatitis(SAP) and explore the underlying mechanism.METHODS SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha(TNf-α), interleukin 6(IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol(1,4,5)-trisphosphate receptor(IP3 R) expression were investigated to assess the mechanism of CEB.RESULTS Pancreatic histopathology score(2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity(2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB(three doses) treatment group compared with the SAP group(2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6(466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α(108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10(200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca2+ concentration, and significantly ameliorated intracellular vacuoles and IP3 m RNA expression compared with those in the SAP group(P < 0.05). There was a trend towards decreased IP3 R protein in the CEB treatment group; however, it did not reach statistical significance(P > 0.05).CONCLUSION These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.
基金Supported by National Natural Sciences Foundation of China,No. 81001067the Ministry of Science and Technology International Cooperation Project, No. 2010DFA31870the AstraZeneca Special Research Foundation for Targeted Therapy of the Wu Jieping Medical Foundation, No. 320.6700.09068
文摘AIM: To investigate the molecular mechanisms underlying the reversal effect of emodin on platinum resistance in hepatocellular carcinoma. METHODS: After the addition of 10 μmol/L emodin to HepG2/oxaliplatin (OXA) cells, the inhibition rate (IR), 50% inhibitory concentration (IC 50 ) and reversal index (IC 50 in experimental group/IC 50 in control group) were calculated. For HepG2, HepG2/OXA, HepG2/OXA/T, each cell line was divided into a control group, OXA group, OXA + fibroblast growth factor 7 (FGF7) group and OXA + emodin group, and the final concentrations of FGF7, emodin and OXA in each group were 5 ng/mL, 10 μg/mL and 10 μmol/L, respectively. Single-cell gel electrophoresis was conducted to detect DNA damage, and the fibroblast growth factor receptor 2 (FGFR2), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and excision repair cross-complementing gene 1 (ERCC1) protein expression levels in each group were examined by Western blotting. RESULTS: Compared with the IC50 of 120.78 μmol/L in HepG2/OXA cells, the IC 50 decreased to 39.65 μmol/L after treatment with 10 μmol/L emodin; thus, the reversal index was 3.05. Compared with the control group, the tail length and Olive tail length in the OXA group, OXA + FGF7 group and OXA + emodin group were significantly increased, and the differences were statistically significant (P < 0.01). The tail length and Olive tail length were lower in the OXA + FGF7 group than in the OXA group, and this difference was also statistically significant. Compared with the OXA + FGF7 group, the tail extent, the Olive tail moment and the percentage of tail DNA were significantly increased in the OXA + emodin group, and these differences were statistically significant (P < 0.01). In comparison with its parental cell line HepG2, the HepG2/OXA cells demonstrated significantly increased FGFR2, p-ERK1/2 and ERCC1 expression levels, whereas the expression of all three molecules was significantly inhibited in HepG2/ OXA/T cells, in which FGFR2 was silenced by FGFR2 shRNA. In the examined HepG2 cells, the FGFR2, p-ERK1/2 and ERCC1 expression levels demonstrated increasing trends in the OXA group and OXA + FGF7 group. Compared with the OXA group and OXA + FGF7 group, the FGFR2, p-ERK1/2, and ERCC1 expression levels were significantly lower in the OXA + emodin group, and these differences were statistically significant. In the HepG2/OXA/T cell line that was transfected with FGFR2 shRNA, the FGFR2, p-ERK1/2 and ERCC1 expression levels were significantly inhibited, but there were no significant differences in these expression levels among the OXA, OXA + FGF7 and OXA + emodin groups. CONCLUSION: Emodin markedly reversed OXA resistance by enhancing OXA DNA damage in HepG2/OXA cells, and the molecular mechanism was related to the inhibitory effect on ERCC1 expression being mediated by the FGFR2/ERK1/2 signaling pathway.
文摘A new series of bone affinity compounds were synthesized by linking emodin with 5-fluorouracil derivatives. Their bone affinities were established by hydroxyapative (HA) affinity experiment in vitro, and their cytostatic effects were shown by the MTT assay.
基金supported by Special Project of Public Welfare Industry Affiliated to Ministry of Health,Grant No:201202011
文摘Objective:To linvestigate the protective effect and mechanism of emodin pretreatment on intestinal mucosa of rats with intestinal ischemia-reperfusion injury.Methods:A total of 50SD rats were randomly divided into control group,model group,emodin groups of low,medium and high dose,with 10 in each group.Ischemia-reperfusion injury(I-RI)mode was established by using noninvasive clamp on superior mesentericartery(SMA).Control group and model group were pretreated with 0.5%sodium carboxymethyl cellulose solution lavage 2 h before operation,emodin groups of low,medium and high dose were given emodin lavage with 20,40,60 mg/kg pretreatment,femoral venous blood before the lavage pretreatment(TO)and 1 h ischemia(Tl),and inferior vena venous blood after 1 h of reperfusion(T2)were extracted from each group of rats for detection of serun level of intestinal fatty acid binding protein(I-FABP),tumor necrosis factor(TNF-α),endotoxin,interleukin 6(IL-6),and die content of diamine oxidase(DAO);Mter model establishment,the rats were sacrificed,intestine homogenate was prepared by using blind intestinal tissue to detect intestinal tissue myeloperoxidase(MPO],malondialdehyde(MDA)and superoxide dismutase(SOD)levels.And upper small intestine tissue was retrieved,followed by fixation and conventional HE staining to observe intestinal tissue morphology under light microscopy.Results:In emodin groups of low,medium and high dose at T1 and T2,I-FABP,TNF-α,endotoxin.IL,-6 and DAO level were significandy lower than that of model group(P<0.05);in emodin group of low,medium and high dose,MPO and MDA content in intestinal tissue homogenate was significantly lower than that in model group(P<0.05),SOD level was significantly higher than that of model group(P<0.05).Intestinal damage of emodin low,medium and high dose groups were significandy lighter than model group.Conclusions:Emodin pretreatment has certain protective effect on intestinal mucosa in ischemia reperfusion injury.
文摘Severe acute pancreatitis accounts for 15% - 20% of acute pancreatitis and is a kind of serious systemic disease because it involves multiple organ damage and dysfunction. Emodin is the most important active ingredient of rhubarb and has been used for the treatment of severe acute pancreatitis. This review mainly summarizes the study progress of emodin in severe acute pancreatitis treatment.
文摘Aim: To explore the emodin’s toxicity and action mechanism on the function of interstitial cells of Cajal (ICC) cultured in vitro. Methods: ICC of KM mouse was cultured in vitro. The minimum toxicity concentration and critical time points of emodin were investigated with Uniform Design methodology and MTT assay. The cell enzymology assay and enzyme immunoassay (EIA) were applied to observe the effect of emodin on membrane stability, cellular internal environment, energy metabolism and second messenger of ICC. Results: The minimum toxicity concentration was 0.001%, and the critical time points were 30 s, 1 min, 30 min, and 60 min. After administration of emodin, the damage on cells aggravated with time prolonging. The activity of malonaldehyde (MDA), lactate dehydrogenase (LDH), and phosphatase in the cell was raised significantly (P + and Ca2+ were increased but K+ concentration was decreased. The Na+-K+-ATPase activity was promoted but Ca2+-ATPase descended. Second messenger as IP3 and cAMP also became more active. All these changes had statistical significance (P Conclusion: Emodin had toxicity function on ICC which can lead to membrane damage, energy metabolism disorder. This mechanism could be related to electrolytes concentration disorder, inhibited activity of Na+-K+-ATPase and Ca2+-ATPase, and raised activity of IP3 and cAMP.
基金supported by Natural Science Foundation of Xuzhou Normal University(No.08XLB08)Science and Technology Project of Xuzhou(No.XJ09078)Universities Natural Science Foundation of Jiangsu Province (No.09KJD 150006)
文摘Hydroxymethylation of 6,8-O-dimethyl emodin was easily achieved in good yields by the modified Marschalk reaction.The influence of the amount of solvent,base and formaldehyde toward the hydroxymethylation was discussed.The results showed that a relatively dilute reaction solution facilitated the generation of the desired 2-hydromethyl product,while the thick reaction solution benefited the generation of the methylated quinizarins.
文摘Over the past years natural products and/or their derivatives have continued to provide cancer chemotherapeutics. Glycosides derivatives of emodin are known to possess anticancer activities. An in silico study was carried out to evaluate emodin derivatives as inhibitors of Arylamine N-Acetyltransferase 2, Cyclooxygenase 2 and Topoisomerase 1 enzymes, predict their pharmacokinetics and explore their bonding modes. Molecular docking study suggested that D2, D5, D6 and D9 to be potent inhibitors of NAT2, while D8 was suggested to be a potent inhibitor of TOP1. Derivatives D2, D5, D6 and D9 bind to the same pocket with different binding conformation. Pharmacokinetic study suggested that selected emodin derivatives can be potential cancer chemotherapeutic agent. Physicochemical parameters such density, balaban index, surface tension, logP and molar reflectance correlated to compounds activity. These finding provides a potential strategy towards developing NAT2 and TOP1 inhibitors.
文摘Cancer is a disease caused by the loss of normal cell regulation and excessive proliferation. At present, there are a lot of anticancer drugs, but most of them are not ideal, with sereve side effects. Besides, during the treatment, the patients feel very bad, and they are always in great pain. Emodin is a natural anthraquinone derivative found in a variety of herbal preparations. Many studies have shown that emodin has a significant therapeutic effect on lung cancer, liver cancer, breast cancer, and so on. After reviewing a large amount of literatures, this paper summarizes the research progresses of emodin anticancer in the past five years, in order to provide theoretical basis for further development and utilization of emodin and its metabolites.
基金supported by National Natural Science Foundation of China,30700151Youth Investigator Fund from UESTC,Y02018023601062
文摘Emodin [1,3,8-Trihydroxy-6-methylanthraquinone] has been reported to exhibit vascular anti-inflammatory properties.However,the relevant anti-inflammatory mechanisms are not well understood.The present study was design to explore the molecular target(s) of emodin
基金Supported by Chinese Medicine and Zhuang and Yao Medicine Hospital Preparation Quality Improvement Project of Guangxi Zhuang Autonomous Region Administration of Traditional Chinese Medicine(GZZJ202013,GZZJ202015)Project of Improving the Scientific Research Basic Ability of Young and Middle-aged Teachers in Guangxi Colleges and Universities in 2019(2019KY0341)+3 种基金Open Project of Guangxi Key Laboratory of Zhuang and Yao Medicine(GXZYKF2020A-08)Scientific Research Project of Guangxi International Zhuang Medicine Hospital in 2020(GZ202001)Youth Foundation Project of Guangxi University of Chinese Medicine in 2019(2019QN036)Zhuang and Yao Medicine Research Laboratory of Guangxi International Zhuang Medicine Hospital.
文摘[Objectives]To establish a method for the determination of emodin in Wudajiangjun liquor,a hospital preparation.[Methods]A high-performance liquid chromatography(HPLC)method for the determination of emodin in Rhizoma Polygontum Cuspidatum in hospital preparation Wudajiangjun liquor was established.Using HPLC method,octadecylsilane chemically bonded silica gel was used as filler for the chromatographic column[Inertsil-C 18 chromatographic column(5μm,4.6 mm×250 mm)].Methanol-0.1%phosphoric acid water(76∶24)was used as mobile phase.The flow rate was 1.0 mL/min,the column temperature was 30℃,the detection wavelength was 254 nm,and the injection volume was 10μL.[Results]The content of emodin in Wudajiangjun liquor was determined by reversed-phase high performance liquid chromatography(RP-HPLC).When the injection volume of emodin was in the range of 5.45-54.5μg/mL,there was a good linear relationship between the injection volume and the peak area.The regression equation is Y=42.952-15.068(r=0.9998),the average recovery rate is 98.23%,and RSD=1.45%.[Conclusions]A method for the determination of emodin in Wudajiangjun liquor by HPLC was established.This method can be used as a quality control method for Wudajiangjun liquor with high accuracy and good repeatability,which lays a foundation for the quality control of the medicinal liquor.
文摘The present study explored quality control of plant drug and polyherbal formulation using HPTLC and HPLC fingerprinting.The study combined qualitative analysis of Emodin and Rhein biomarker compound in Rhei Emodi Wall.rhizome extract and polyherbal formulation extract by HPTLC method with quantitative estimation of Emodin by HPLC method,aiming to help in accurate identification of Emodin and Rhein in plant materials,polyherbal formulations.This study also checked adulteration,with the purpose of improving bio-efficacy of ayurvedic formulation.All the samples showed characteristic peaks of Emodin at same retention time as that of standard Emodin.According to the HPTLC fingerprinting results,the Rf values of Rhein reference standard at 0.42 and Emodin at 0.62 were observed in test solution of Rhei emodi Wall.rhizome extract and polyherbal formulation extract and both were found comparable.The quantitative evaluation of Emodin present in the polyherbal formulation and Rhei emodi Wall.rhizome extracts were 0.0177% and 0.3106% respectively.
基金Supported by Key Research Projects of Hubei Province, No.2002AA302B13
文摘AIM: To investigate the effects of emodin on the treatment of non-alcoholic fatty liver in rats induced by high caloric laboratory chaw.METHODS: Non-alcoholic fatty liver model was successfully established by feeding with high caloric laboratory chaw for 12 wk. Then the model rats were randomly divided into 3 groups, namely model control group, emodin group and dietary treatment group. The rats in emodin group in othergroups were given distilled water of the same volume. The rats in model control group were fed with high caloric laboratory chaw while animals in other groups were fed with normal diet. Four weeks later, liver index (liver/body weight ratio), serum activities of liver-associated enzymes, blood lipid, fasting blood glucose, fasting plasma insulin, HOMA insulin resistance index (HOMA-IR), hepatic triglyceride content and histology features of all groups were assayed. The expression of hepatic peroxisomal proliferator activated receptor (PPAR) gamma was determined by RT-PCR.RESULTS: The body weight, liver index, serum activities of alanine aminotransferase (ALT), blood lipid, hepatic triglyceride content of model control group were significantly elevated, with moderate to severe hepatocyte steatosis.The expression of hepatic PPAR gamma mRNA was obviously reduced in model control group. Compared with model control group, the body weight, liver index, serum activities of ALT, blood lipids and hepatic triglyceride of emodin group significantly decreased and hepatic histology display was also greatly improved. Meanwhile, the expression of hepatic PPAR gamma mRNA was elevated.However, high serum activities of ALT and hyperlipidemia were persisted in dietary treatment group although liver index was decreased and liver histology was somewhat improved.CONCLUSION: It is suggested that emodin might be effective in the treatment of non-alcoholic fatty liver in rats. Its therapeutic mechanism could be associated with increasing the expression of hepatic PPAR gamma mRNA.
