BACKGROUND Jianpi Gushen Huayu Decoction(JPGS)has been used to clinically treat diabetic nephropathy(DN)for many years.However,the protective mechanism of JPGS in treating DN remains unclear.AIM To evaluate the therap...BACKGROUND Jianpi Gushen Huayu Decoction(JPGS)has been used to clinically treat diabetic nephropathy(DN)for many years.However,the protective mechanism of JPGS in treating DN remains unclear.AIM To evaluate the therapeutic effects and the possible mechanism of JPGS on DN.METHODS We first evaluated the therapeutic potential of JPGS on a DN mouse model.We then investigated the effect of JPGS on the renal metabolite levels of DN mice using non-targeted metabolomics.Furthermore,we examined the effects of JPGS on c-Jun N-terminal kinase(JNK)/P38-mediated apoptosis and the inflammatory responses mediated by toll-like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)/NOD-like receptor family pyrin domain containing 3(NLRP3).RESULTS The ameliorative effects of JPGS on DN mice included the alleviation of renal injury and the control of inflammation and oxidative stress.Untargeted metabolomic analysis revealed that JPGS altered the metabolites of the kidneys in DN mice.A total of 51 differential metabolites were screened.Pathway analysis results indicated that nine pathways significantly changed between the control and model groups,while six pathways significantly altered between the model and JPGS groups.Pathways related to cysteine and methionine metabolism;alanine,tryptophan metabolism;aspartate and glutamate metabolism;and riboflavin metabolism were identified as the key pathways through which JPGS affects DN.Further experimental validation showed that JPGS treatment reduced the expression of TLR4/NF-κB/NLRP3 pathways and JNK/P38 pathway-mediated apoptosis related factors.CONCLUSION JPGS could markedly treat mice with streptozotocin(STZ)-induced DN,which is possibly related to the regulation of several metabolic pathways found in kidneys.Furthermore,JPGS could improve kidney inflammatory responses and ameliorate kidney injuries in DN mice via the TLR4/NF-κB/NLRP3 pathway and inhibit JNK/P38 pathwaymediated apoptosis in DN mice.展开更多
Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-i...Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.展开更多
Background:To clarify the inhibitory effect of Ercao Qinggan decoction(EQD)on acute liver failure(ALF)and its related mechanisms.Methods:HL-7702 hepatocytes were pretreated with TLR4 inhibitor CLI-095,glycogen synthas...Background:To clarify the inhibitory effect of Ercao Qinggan decoction(EQD)on acute liver failure(ALF)and its related mechanisms.Methods:HL-7702 hepatocytes were pretreated with TLR4 inhibitor CLI-095,glycogen synthase kinase 3β(GSK3β)inhibitor LiCl and different doses of EQD for 2 hours,and lipopolysaccharide(LPS)(10μg/mL)for 24 hours.Cell apoptosis,TNF-αand IL-6 and GSK3βwere detected by flow cytometry,immunofluorescence,quantitative polymerase chain reaction.After mice were gavaged with different concentrations of EQD for 12 days,ALF mouse models were established intraperitoneal injection of D-Gal/LPS.After 24 hours,the mice were euthanized and the liver tissue was stained with hematoxylin and eosin.Liver cell apoptosis,the serum levels of aspartate aminotransferase,alanine aminotransferase,TNF-αand IL-βwere detected by terminal transferase-mediated dUTP nick end-labelling,enzyme linked immunosorbent assay,quantitative polymerase chain reaction,and Western blotting,respectively.These methods were also used to test the mRNA expression of Bax,Bcl-2 and the protein expression of GSK3β,p-Akt/Akt in livers.Results:CLI-095,LiCl,and EQD significantly inhibited apoptosis induced by LPS,the mRNA expression of IL-6,TNF-αand the nuclear translocation of GSK3βin HL-7702 hepatocytes.EQD dose-dependently inhibited hepatocyte apoptosis,the serum concentration of aspartate aminotransferase and ALT,the expression of TNF-αand IL-β,the ratio of p-GSK3β/GSK3β,p-Akt/Akt in alanine aminotransferase mice.Conclusion:EQD can inhibit hepatocyte apoptosis in ALF mice through regulating TLR4/PI3K/Akt/GSK3βsignaling pathway.展开更多
Objective:To observe the effect of Sanshi decoction on BRD4/NF-κB/NLRP3 pathwaymediated macrophage pyroptosis,so as to elucidate the molecular mechanism of Sanshi decoction in the treatment of gouty arthritis.Methods...Objective:To observe the effect of Sanshi decoction on BRD4/NF-κB/NLRP3 pathwaymediated macrophage pyroptosis,so as to elucidate the molecular mechanism of Sanshi decoction in the treatment of gouty arthritis.Methods:THP-1 was induced into macrophages with foboside and the divided into the control group,model group,low-dose,medium-dose,high-dose group of Sanshi decoction,and BRD4 inhibitor group.Except for the control group,the remaining groups were induced with monosodium urate crystals to construct a gouty arthritis cell model.The activity of macrophages was detected by CCK8,the level of macrophage pyroptosis was detected by flow cytometry,the activity of LDH,the content of IL-1β and IL-18 were detected by enzyme-linked immunosorbent assay,and the expression of related proteins in the BRD4/NF-κB/NLRP3 pathway was detected by Western blot.Results:Compared with the control group,macrophage activity was decreased in the model group,and the level of pyroptosis,LDH activity,contents of IL-1β and IL-18,expression levels of BRD4,p-NF-kB p65,NLRP3,Caspase-1 p20,and IL-1β protein were significantly up-regulated,the differences were statistically significant(P<0.05 and P<0.01).Compared with the model group,macrophage activity was up-regulated in the Sanshi Decoction,and the level of pyroptosis,LDH activity,IL-1β and IL-18 contents,expression levels of BRD4,p-NF-kB p65,NLRP3,Caspase-1 p20,and IL-1β protein were significantly decreased with statistically significant differences(P<0.05 and P<0.01).Conclusion:Sanshi decoction inhibits macrophage pyroptosis by inhibiting BRD4/NF-κB/NLRP3 pathway activation,thus improving the inflammation level of gouty arthritis.展开更多
Background:The objective of this research was to examine the impact of the Chinese herbal formula Qushi Kaiyu(QSKY)on rats with non-alcoholic fatty liver disease(NAFLD)and its inhibitory effect on the TLR4/NF-ĸB pathw...Background:The objective of this research was to examine the impact of the Chinese herbal formula Qushi Kaiyu(QSKY)on rats with non-alcoholic fatty liver disease(NAFLD)and its inhibitory effect on the TLR4/NF-ĸB pathway.Methods:NAFLD model rats was constructed through high-fat diet.Meanwhile,rats were treated with QSKY(6.4 g/kg)by gavage.The therapeutic effect of QSKY on NAFLD was assessed by testing body weight change,the liver index,lipid concentrations in blood,and antioxidant and inflammatory levels;assessing liver function;and performing pathological staining including hematoxylin-eosin and Oil Red O.The protein levels of key factors in the TLR4/NF-ĸB pathway(TLR4,MyD88,p65 and IKB)in rat liver tissue were determined using western blotting in order to explore the mechanism responsible for the therapeutic effects of QSKY in rats with NAFLD.Results:QSKY significantly reduced the liver index and body weight value;reduced triglyceride,cholesterol,alanine aminotransferase,and aspartate aminotransferase levels in NAFLD rats;improved the pathological changes,such as ballooning degeneration,fat accumulation,necrosis,and inflammation;elevated GSH-Px and superoxide dismutase activities and lowered malondialdehyde levels,indicating that QSKY enhanced the antioxidant capacity;and reduced inflammatory cytokine(IL-6,IL-1β,and TNF-α)levels.Western blotting results showed that QSKY significantly reduced TLR4,MyD88,and decreased the phosphorylation of IKB and p65 protein levels in the livers of rats with NAFLD.Conclusions:QSKY showed therapeutic effects on NAFLD and can alleviate oxidative stress and inflammation.This mechanism may be related to an improvement in TLR4/NF-ĸB pathway.展开更多
Objective: The aim of the study was to observe the clinical efficacy with Yiqi Jianpi decoction combination with FOLFOX4 for the postoperative patients of colorectal cancer (CRC). Methods: Eighty-five patients were ra...Objective: The aim of the study was to observe the clinical efficacy with Yiqi Jianpi decoction combination with FOLFOX4 for the postoperative patients of colorectal cancer (CRC). Methods: Eighty-five patients were randomly divided into two groups. The treated group (n = 41) received Yiqi Jianpi decoction combined with FOLFOX4 chemotherapy and the control group (n = 44) received FLOFOX4 chemotherapy alone. A treatment course of 6 months was applied to both groups. Results: The life quality, symptomatic improvement and adverse side effects reducing in the treated group were better than those of the control group. Conclusion: Yiqi Jianpi decoction combination with FOLFOX4 chemotherapy is effective in the treatment of the postoperative patients with colorectal cancer.展开更多
Objective To explore the effect and mechanism of Chaihu Longgu Muli Decoction(柴胡龙骨牡蛎汤,CHLGMLD)in rats with temporal lobe epilepsy(TLE).Methods A total of 80 Sprague-Dawley(SD)male rats were randomized into cont...Objective To explore the effect and mechanism of Chaihu Longgu Muli Decoction(柴胡龙骨牡蛎汤,CHLGMLD)in rats with temporal lobe epilepsy(TLE).Methods A total of 80 Sprague-Dawley(SD)male rats were randomized into control(CON),model(MOD),carbamazepine(CBZ,0.1 g/kg),CHLGMLD low dose(CHLGMLD-L,12.5 g/kg),and high dose(CHLGMLD-H,25 g/kg)groups,with 16 rats in each group.TLE rat models were established in the four groups with the use of lithium-pilocarpine except for the CON group.After the successful establishment of TLE models,all drugs were administered through gavage,and distilled water was given to rats in the CON and MOD groups for four weeks.The frequency and duration of seizures before and after treatment were recorded for the evaluation of the alleviation degree.Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the expression levels of miR-146a-3p and miR-146a-5p.The expression levels of toll-like receptor 4(TLR4),interleukin-1 receptor-associated kinase 1(IRAK1),tumor necrosis factor(TNF)receptor-associated factor 6(TRAF6),TAK1-binding protein(TAB),nuclear factor-kappa B(NF-κB),and interleukin-1 beta(IL-1β)in hippocampus were tested by immunofluorescence assay.Correlation analysis between the above factors and expressions of miR-146a-3p and miR-146a-5p were performed separately.Results CHLGMLD decreased the frequency(P<0.05)and duration(P<0.01)of seizures in rats.CHLGMLD down-regulated the expression levels of miR-146a-5p and miR-146a-3p(P<0.05),and inhibited the expression levels of TLR4,IRAK1,TRAF6,TAB,NF-κB,and IL-1β(P<0.01).The correlation analysis revealed that the expression levels of TLR4,IRAK1,TRAF6,TAB,NF-κB,and IL-1β were positively correlated with the expression levels of miR-146a-3p and miR-146a-5p detected by qRT-PCR,respectively(P<0.01).Conclusion CHLGMLD can inhibite the TLR4 signaling pathway by lowering the expression levels of miR-146a-3p and miR-146a-5p to alleviate hippocampal dentate gyrus inflammation in TLE rats,thus relieving seizures.展开更多
Objective:The aim of the study was to observe the therapeutic effect of FOLFOX4 regimen plus Fufangchangtai decoction on postoperative colorectal cancers.Methods:Thirty postoperative colorectal cancer patients were al...Objective:The aim of the study was to observe the therapeutic effect of FOLFOX4 regimen plus Fufangchangtai decoction on postoperative colorectal cancers.Methods:Thirty postoperative colorectal cancer patients were allocated into control and experiment groups respectively.Patients in experiment group were given Fufangchangtai decoction combined with FOLFOX4 regimen.Patients in control group were given FOLFOX4 regimen alone.Efficacy was evaluated after 2 periods of treatment.Results:The improvement rate of symptoms were 86.6% in experiment group compared to 53.3% in control group.KPS was stable in experiment group,and decreased in control group.QOL was increased in experiment group,and stable in control group after the treatment.For impact of immunity parameters,there were enhancements of CD3+ and CD4+ in experiment group,while they did not change in control group.In experiment group,WBC reduction was slighter than that of control group.The differences were not remarkable in PLT reduction,alimentary response,and toxicity of liver and kidney and nervous system.Conclusion:The clinical observation showed that Fufangchangtai decoction plus FOLFOX4 regimen could effectively enhance KPS,improve the symptoms,the quality of life and the immunity state,and down-regulate the side effects.In conclusion,Fufangchangtai decoction can decrease the toxicity so as to increase the treatment effect.展开更多
[Objectives] To explore the effect of Buyanghuanwu decoction on PI3K/AKT signaling pathway and aquaporin AQP4 in cerebral hemorrhage rats and clarify the mechanism to provide clear direction and target for cerebral he...[Objectives] To explore the effect of Buyanghuanwu decoction on PI3K/AKT signaling pathway and aquaporin AQP4 in cerebral hemorrhage rats and clarify the mechanism to provide clear direction and target for cerebral hemorrhage treatment caused by cerebral edema.[Methods]SD rats were randomly divided into six groups: model group,sham operation group,Buyanghuanwu decoction low,medium and high dose groups,and Ginkgo biloba group. Model group,Buyanghuanwu decoction group,G. biloba group were prepared to be intracerebral hemorrhage rat models by referring to Rosenberg law. While the expression of " polarity" of aquaporin AQP4 was detected by immunofluorescence labeling method,the Evans blue( Evans Blue,EB) content of brain tissue was determined by Spectrophotometry. In addition,the water content of brain tissue was detected by wet and dry weight method. [Results] When compared to the model group,the Buyang Huanwu decoction group,G. biloba group of PI3K and AKT proteins expression increased significantly( P < 0. 05) and AQP4 in Astrocyte end feet membrane concentrated expression significantly increased( P < 0. 05),EB content and water content of brain tissue significantly reduced( P <0. 05).[Conclusions]The protective mechanisms of Buyanghuanwu decoction on cerebral hemorrhage can work might because it can activate PI3K/AKT signaling pathway,regulate AQP4 " polar" expression,and reduce the permeability of the blood brain barrier and cerebral edema.展开更多
基金Supported by the Scientific Foundation of Administration of Traditional Chinese Medicine of Hebei Province,China,No.2023257.
文摘BACKGROUND Jianpi Gushen Huayu Decoction(JPGS)has been used to clinically treat diabetic nephropathy(DN)for many years.However,the protective mechanism of JPGS in treating DN remains unclear.AIM To evaluate the therapeutic effects and the possible mechanism of JPGS on DN.METHODS We first evaluated the therapeutic potential of JPGS on a DN mouse model.We then investigated the effect of JPGS on the renal metabolite levels of DN mice using non-targeted metabolomics.Furthermore,we examined the effects of JPGS on c-Jun N-terminal kinase(JNK)/P38-mediated apoptosis and the inflammatory responses mediated by toll-like receptor 4(TLR4)/nuclear factor-kappa B(NF-κB)/NOD-like receptor family pyrin domain containing 3(NLRP3).RESULTS The ameliorative effects of JPGS on DN mice included the alleviation of renal injury and the control of inflammation and oxidative stress.Untargeted metabolomic analysis revealed that JPGS altered the metabolites of the kidneys in DN mice.A total of 51 differential metabolites were screened.Pathway analysis results indicated that nine pathways significantly changed between the control and model groups,while six pathways significantly altered between the model and JPGS groups.Pathways related to cysteine and methionine metabolism;alanine,tryptophan metabolism;aspartate and glutamate metabolism;and riboflavin metabolism were identified as the key pathways through which JPGS affects DN.Further experimental validation showed that JPGS treatment reduced the expression of TLR4/NF-κB/NLRP3 pathways and JNK/P38 pathway-mediated apoptosis related factors.CONCLUSION JPGS could markedly treat mice with streptozotocin(STZ)-induced DN,which is possibly related to the regulation of several metabolic pathways found in kidneys.Furthermore,JPGS could improve kidney inflammatory responses and ameliorate kidney injuries in DN mice via the TLR4/NF-κB/NLRP3 pathway and inhibit JNK/P38 pathwaymediated apoptosis in DN mice.
基金National Natural Science Foundation of China(grant numbers 82174143)the Innovative Team Project of Ordinary Universities in Guangdong Province(grant numbers 2022KCXTD016).
文摘Background:Liu-Jun-Zi decoction(LJZD),a classical nourishing formula in China,has been proven to be effective in treating chemotherapy-induced anorexia.In this study,the mechanism of LJZD in alleviating chemotherapy-induced anorexia was discussed from the aspects of regulating gut microbiota,repairing intestinal barrier injury and inhibiting inflammatory pathways.Methods:A rat model of chemotherapy-induced anorexia was established using cisplatin.The study evaluated the therapeutic effects of LJZD by observing the weight,food intake,and intestinal pathology of rats.The impact of LJZD on gut microbiota and metabolites,specifically short-chain fatty acids,was investigated through gut microbiota analysis and targeted metabolomics.The anti-inflammatory and intestinal protective effects of LJZD were assessed by examining the expression of intestinal tight junction proteins associated with the inflammatory pathway.Results:LJZD alleviated cisplatin-induced inflammation and intestinal barrier disruption,as evidenced by upregulated expression of tight junction protein 1(TJ-1)and occludin,along with reduced serum levels of interleukin 6(IL-6),interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and lipopolysaccharide.Additionally,LJZD alleviated microbiota imbalance and regulated the levels of short-chain fatty acids,especially increased the relative abundance of Coriobacteriales Incertae Sedis,Lactabacillus johnsonii F19785,Parasutterella,and reduced the Tyzzerella.In the hypothalamus,LJZD exerts suppressive effects on the toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor-κB(NF-κB)p65 signaling pathway,leading to a downregulation in the transcriptional activity of IL-6 and IL-1β,as well as Interleukin 6 receptors(IL-6R)and Interleukin-1βreceptors(IL-1R1)mRNA expression levels.Conclusion:In summary,LJZD alleviate chemotherapy-induced anorexia by modulating the gut microbiota,repairing the intestinal mechanical barriers,and suppressing the TLR4/MyD88/NF-κB p65 signaling pathway.
基金The National Natural Science Foundation of Zhejiang Provincial(No.LGF21H270001)the Association of Integrated Chinese and Western Medicine Research Fund Project of Zhejiang Provincial(No.2019LY013)the Basic Research Project of Wenzhou Science and Technology Bureau(No.Y20210149)supported this study.
文摘Background:To clarify the inhibitory effect of Ercao Qinggan decoction(EQD)on acute liver failure(ALF)and its related mechanisms.Methods:HL-7702 hepatocytes were pretreated with TLR4 inhibitor CLI-095,glycogen synthase kinase 3β(GSK3β)inhibitor LiCl and different doses of EQD for 2 hours,and lipopolysaccharide(LPS)(10μg/mL)for 24 hours.Cell apoptosis,TNF-αand IL-6 and GSK3βwere detected by flow cytometry,immunofluorescence,quantitative polymerase chain reaction.After mice were gavaged with different concentrations of EQD for 12 days,ALF mouse models were established intraperitoneal injection of D-Gal/LPS.After 24 hours,the mice were euthanized and the liver tissue was stained with hematoxylin and eosin.Liver cell apoptosis,the serum levels of aspartate aminotransferase,alanine aminotransferase,TNF-αand IL-βwere detected by terminal transferase-mediated dUTP nick end-labelling,enzyme linked immunosorbent assay,quantitative polymerase chain reaction,and Western blotting,respectively.These methods were also used to test the mRNA expression of Bax,Bcl-2 and the protein expression of GSK3β,p-Akt/Akt in livers.Results:CLI-095,LiCl,and EQD significantly inhibited apoptosis induced by LPS,the mRNA expression of IL-6,TNF-αand the nuclear translocation of GSK3βin HL-7702 hepatocytes.EQD dose-dependently inhibited hepatocyte apoptosis,the serum concentration of aspartate aminotransferase and ALT,the expression of TNF-αand IL-β,the ratio of p-GSK3β/GSK3β,p-Akt/Akt in alanine aminotransferase mice.Conclusion:EQD can inhibit hepatocyte apoptosis in ALF mice through regulating TLR4/PI3K/Akt/GSK3βsignaling pathway.
基金Heilongjiang Province Tradit Chin Med Research Projec(No.ZHY19-006)。
文摘Objective:To observe the effect of Sanshi decoction on BRD4/NF-κB/NLRP3 pathwaymediated macrophage pyroptosis,so as to elucidate the molecular mechanism of Sanshi decoction in the treatment of gouty arthritis.Methods:THP-1 was induced into macrophages with foboside and the divided into the control group,model group,low-dose,medium-dose,high-dose group of Sanshi decoction,and BRD4 inhibitor group.Except for the control group,the remaining groups were induced with monosodium urate crystals to construct a gouty arthritis cell model.The activity of macrophages was detected by CCK8,the level of macrophage pyroptosis was detected by flow cytometry,the activity of LDH,the content of IL-1β and IL-18 were detected by enzyme-linked immunosorbent assay,and the expression of related proteins in the BRD4/NF-κB/NLRP3 pathway was detected by Western blot.Results:Compared with the control group,macrophage activity was decreased in the model group,and the level of pyroptosis,LDH activity,contents of IL-1β and IL-18,expression levels of BRD4,p-NF-kB p65,NLRP3,Caspase-1 p20,and IL-1β protein were significantly up-regulated,the differences were statistically significant(P<0.05 and P<0.01).Compared with the model group,macrophage activity was up-regulated in the Sanshi Decoction,and the level of pyroptosis,LDH activity,IL-1β and IL-18 contents,expression levels of BRD4,p-NF-kB p65,NLRP3,Caspase-1 p20,and IL-1β protein were significantly decreased with statistically significant differences(P<0.05 and P<0.01).Conclusion:Sanshi decoction inhibits macrophage pyroptosis by inhibiting BRD4/NF-κB/NLRP3 pathway activation,thus improving the inflammation level of gouty arthritis.
基金Study on the mechanism of Qushi Kaiyu Decoction in regulating intestinal flora to alleviate chronic inflammation in the treatment of nonalcoholic fatty liver disease(2022AD10005).
文摘Background:The objective of this research was to examine the impact of the Chinese herbal formula Qushi Kaiyu(QSKY)on rats with non-alcoholic fatty liver disease(NAFLD)and its inhibitory effect on the TLR4/NF-ĸB pathway.Methods:NAFLD model rats was constructed through high-fat diet.Meanwhile,rats were treated with QSKY(6.4 g/kg)by gavage.The therapeutic effect of QSKY on NAFLD was assessed by testing body weight change,the liver index,lipid concentrations in blood,and antioxidant and inflammatory levels;assessing liver function;and performing pathological staining including hematoxylin-eosin and Oil Red O.The protein levels of key factors in the TLR4/NF-ĸB pathway(TLR4,MyD88,p65 and IKB)in rat liver tissue were determined using western blotting in order to explore the mechanism responsible for the therapeutic effects of QSKY in rats with NAFLD.Results:QSKY significantly reduced the liver index and body weight value;reduced triglyceride,cholesterol,alanine aminotransferase,and aspartate aminotransferase levels in NAFLD rats;improved the pathological changes,such as ballooning degeneration,fat accumulation,necrosis,and inflammation;elevated GSH-Px and superoxide dismutase activities and lowered malondialdehyde levels,indicating that QSKY enhanced the antioxidant capacity;and reduced inflammatory cytokine(IL-6,IL-1β,and TNF-α)levels.Western blotting results showed that QSKY significantly reduced TLR4,MyD88,and decreased the phosphorylation of IKB and p65 protein levels in the livers of rats with NAFLD.Conclusions:QSKY showed therapeutic effects on NAFLD and can alleviate oxidative stress and inflammation.This mechanism may be related to an improvement in TLR4/NF-ĸB pathway.
文摘Objective: The aim of the study was to observe the clinical efficacy with Yiqi Jianpi decoction combination with FOLFOX4 for the postoperative patients of colorectal cancer (CRC). Methods: Eighty-five patients were randomly divided into two groups. The treated group (n = 41) received Yiqi Jianpi decoction combined with FOLFOX4 chemotherapy and the control group (n = 44) received FLOFOX4 chemotherapy alone. A treatment course of 6 months was applied to both groups. Results: The life quality, symptomatic improvement and adverse side effects reducing in the treated group were better than those of the control group. Conclusion: Yiqi Jianpi decoction combination with FOLFOX4 chemotherapy is effective in the treatment of the postoperative patients with colorectal cancer.
基金National Natural Science Foundation of China(81874429)Natural Science Foundation of Hunan Province(2020JJ5294)+3 种基金Traditional Chinese Medicine Science&Research Project of Hunan Province(202145)Excellent Youth Program of Hunan Education Department(21B0081)Hunan Provincial Administration of Traditional Chinese Medicine(D2022027)Changsha Natural Science Foundation of China(KQ2202255).
文摘Objective To explore the effect and mechanism of Chaihu Longgu Muli Decoction(柴胡龙骨牡蛎汤,CHLGMLD)in rats with temporal lobe epilepsy(TLE).Methods A total of 80 Sprague-Dawley(SD)male rats were randomized into control(CON),model(MOD),carbamazepine(CBZ,0.1 g/kg),CHLGMLD low dose(CHLGMLD-L,12.5 g/kg),and high dose(CHLGMLD-H,25 g/kg)groups,with 16 rats in each group.TLE rat models were established in the four groups with the use of lithium-pilocarpine except for the CON group.After the successful establishment of TLE models,all drugs were administered through gavage,and distilled water was given to rats in the CON and MOD groups for four weeks.The frequency and duration of seizures before and after treatment were recorded for the evaluation of the alleviation degree.Quantitative real-time polymerase chain reaction(qRT-PCR)was used to detect the expression levels of miR-146a-3p and miR-146a-5p.The expression levels of toll-like receptor 4(TLR4),interleukin-1 receptor-associated kinase 1(IRAK1),tumor necrosis factor(TNF)receptor-associated factor 6(TRAF6),TAK1-binding protein(TAB),nuclear factor-kappa B(NF-κB),and interleukin-1 beta(IL-1β)in hippocampus were tested by immunofluorescence assay.Correlation analysis between the above factors and expressions of miR-146a-3p and miR-146a-5p were performed separately.Results CHLGMLD decreased the frequency(P<0.05)and duration(P<0.01)of seizures in rats.CHLGMLD down-regulated the expression levels of miR-146a-5p and miR-146a-3p(P<0.05),and inhibited the expression levels of TLR4,IRAK1,TRAF6,TAB,NF-κB,and IL-1β(P<0.01).The correlation analysis revealed that the expression levels of TLR4,IRAK1,TRAF6,TAB,NF-κB,and IL-1β were positively correlated with the expression levels of miR-146a-3p and miR-146a-5p detected by qRT-PCR,respectively(P<0.01).Conclusion CHLGMLD can inhibite the TLR4 signaling pathway by lowering the expression levels of miR-146a-3p and miR-146a-5p to alleviate hippocampal dentate gyrus inflammation in TLE rats,thus relieving seizures.
基金Supported by a grant from the Natural Science Foundation of Jiangsu Province, China (No. BK2006156)
文摘Objective:The aim of the study was to observe the therapeutic effect of FOLFOX4 regimen plus Fufangchangtai decoction on postoperative colorectal cancers.Methods:Thirty postoperative colorectal cancer patients were allocated into control and experiment groups respectively.Patients in experiment group were given Fufangchangtai decoction combined with FOLFOX4 regimen.Patients in control group were given FOLFOX4 regimen alone.Efficacy was evaluated after 2 periods of treatment.Results:The improvement rate of symptoms were 86.6% in experiment group compared to 53.3% in control group.KPS was stable in experiment group,and decreased in control group.QOL was increased in experiment group,and stable in control group after the treatment.For impact of immunity parameters,there were enhancements of CD3+ and CD4+ in experiment group,while they did not change in control group.In experiment group,WBC reduction was slighter than that of control group.The differences were not remarkable in PLT reduction,alimentary response,and toxicity of liver and kidney and nervous system.Conclusion:The clinical observation showed that Fufangchangtai decoction plus FOLFOX4 regimen could effectively enhance KPS,improve the symptoms,the quality of life and the immunity state,and down-regulate the side effects.In conclusion,Fufangchangtai decoction can decrease the toxicity so as to increase the treatment effect.
基金Supported by 2018 National Undergraduate Innovation and Entrepreneurship Training Program of Chengde Medical College(2018004)Key Medicinal Research Project of Hebei Provincial Department of Public Health(20170872)
文摘[Objectives] To explore the effect of Buyanghuanwu decoction on PI3K/AKT signaling pathway and aquaporin AQP4 in cerebral hemorrhage rats and clarify the mechanism to provide clear direction and target for cerebral hemorrhage treatment caused by cerebral edema.[Methods]SD rats were randomly divided into six groups: model group,sham operation group,Buyanghuanwu decoction low,medium and high dose groups,and Ginkgo biloba group. Model group,Buyanghuanwu decoction group,G. biloba group were prepared to be intracerebral hemorrhage rat models by referring to Rosenberg law. While the expression of " polarity" of aquaporin AQP4 was detected by immunofluorescence labeling method,the Evans blue( Evans Blue,EB) content of brain tissue was determined by Spectrophotometry. In addition,the water content of brain tissue was detected by wet and dry weight method. [Results] When compared to the model group,the Buyang Huanwu decoction group,G. biloba group of PI3K and AKT proteins expression increased significantly( P < 0. 05) and AQP4 in Astrocyte end feet membrane concentrated expression significantly increased( P < 0. 05),EB content and water content of brain tissue significantly reduced( P <0. 05).[Conclusions]The protective mechanisms of Buyanghuanwu decoction on cerebral hemorrhage can work might because it can activate PI3K/AKT signaling pathway,regulate AQP4 " polar" expression,and reduce the permeability of the blood brain barrier and cerebral edema.
