Objective:The aim of this study is to investigate the effects of Hepatocyte Growth Factor(HGF)on the expression levels of IL-8,TNF-α,IL-4,and IL-21 in mice with liver injury induced by CCL_(4).Methods:An acute liver ...Objective:The aim of this study is to investigate the effects of Hepatocyte Growth Factor(HGF)on the expression levels of IL-8,TNF-α,IL-4,and IL-21 in mice with liver injury induced by CCL_(4).Methods:An acute liver injury mouse model was established using CCL_(4),and hepatocytes and white blood cells were separated by gradient density centrifugation.Different concentrations of HGF were added in vitro,and the expression levels of cytokines were detected using ELISA.Results:In the in vivo injury model,the hepatocyte experiment results showed that the expression level of IL-8 was reduced in the 10 ng/mL HGF group compared to the injured hepatocyte group(P<0.05),and increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.05).For IL-4,the expression levels were reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the injured hepatocyte group.The white blood cell experiment results showed that the expression levels of TNF-αwere reduced in both the 10ng/ml HGF group(P<0.05)and the 25 ng/mL HGF group(P<0.05)compared to the injured white blood cell group.In the in vitro injury model,hepatocyte experiment results showed that the expression levels of TNF-αwere reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the normal control group.For IL-4,the expression level was reduced in the 25 ng/mL HGF group compared to the normal control group(P<0.05).The white blood cell experiment results showed that the expression level of TNF-αwas increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.001);for IL-21,the expression levels were reduced in the CCL_(4) model group(P<0.05),10 ng/mL HGF group(P<0.05),25 ng/mL HGF group(P<0.05),and 50 ng/mL HGF group(P<0.05)compared to the normal control group.Conclusion:when the liver of mice is acutely damaged by CCL_(4),HGF can reduce the expression levels of inflammatory cytokines IL-8,TNF-α,IL-4 in hepatocytes,and TNF-αin liver white blood cells.展开更多
[Objectives]To explore the protective effects of flavonoids from Pteridium aquilinum(PAFL)on carbon tetracholoride(CCl_(4))-induced acute liver injury in mice and its potential mechanism.[Methods]All mice were randoml...[Objectives]To explore the protective effects of flavonoids from Pteridium aquilinum(PAFL)on carbon tetracholoride(CCl_(4))-induced acute liver injury in mice and its potential mechanism.[Methods]All mice were randomly divided into four groups(n=10 in each),normal group,CCl_(4)group,CCl_(4)+PAFL groups[treated with PAFL(50 or 200 mg/kg)].Animal treatment was continued for 7 consecutive days.The blood was collected after injection of CCl_(4)for 24 h,and the liver tissue was removed from the mice and stored at-80℃.[Results]The PAFL(50 and 200 mg/kg)significantly inhibited the increase of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)levels in serum caused by CCl_(4)treatment.PAFL administration not only increased the activity of antioxidant enzymes superoxide dismutase(SOD),Glutathione(GSH)and catalase(CAT)in mice,but also reduced the level of malondialdehyde(MDA).Meanwhile,PAFL administration decreased the expression of nuclear factor-kappa B(NF-κB)and Cyclooxygenase-2(COX-2)proteins and inhibited the release of pro-inflammatory factors tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin 6(IL-6).In addition,PAFL(200 mg/kg)treatment down-regulated extracellular regulated protein kinases(ERK)and c-Jun N-terminal kinase(JNK)protein levels in liver tissue.[Conclusions]These findings clearly indicate that the protective effects of PAFL on CCl_(4)-induced acute liver injury is related to its antioxidant and anti-inflammatory activity,which may be mediated by NF-κB and MAPKs signaling pathways.展开更多
研究黄精(Polygonatumsibiricum,PS)对CCl_(4)诱导的大鼠肝损伤的保护作用及其抗氧化机制。采用一次性腹腔注射50%四氯化碳油溶液建立大鼠急性肝损伤模型,用黄精水提物(PSAE)灌胃治疗,水飞蓟素作为阳性对照药物,连续7天。PSAE显著降低...研究黄精(Polygonatumsibiricum,PS)对CCl_(4)诱导的大鼠肝损伤的保护作用及其抗氧化机制。采用一次性腹腔注射50%四氯化碳油溶液建立大鼠急性肝损伤模型,用黄精水提物(PSAE)灌胃治疗,水飞蓟素作为阳性对照药物,连续7天。PSAE显著降低了血清丙氨酸转氨酶、天冬氨酸转氨酶和碱性磷酸酶(AST、ALT和ALP)的水平(P<0.05),增加了肝组织谷胱甘肽(GSH)和超氧化物歧化酶(T-SOD)的水平(P<0.05),降低了肝组织中丙二醛的活性(P<0.05),并显著降低了肝细胞中的活性氧水平(P<0.05)。在肝组织中,核因子类红细胞2相关因子2(Nrf2),NAD(P)H醌脱氢酶1(NQO-1),血红素加氧酶1(HO-1)mRNA的表达水平显著升高,p53 mRNA表达显著降低(P<0.05),Bcl-2(P<0.05)和Bcl-x L mRNA的表达升高,HO-1蛋白表达升高,Keap-1 mRNA表达无明显差异(P>0.05)。因此,黄精对CCl_(4)诱导的急性肝损伤有较好的保护作用,其机制与有效调节Nrf2-Keap1-ARE通路相关基因和蛋白质的表达、抑制p53途径介导的肝细胞凋亡有关。展开更多
基金Natural Science Foundation of Hainan Province(No.821QN0893)Natural Science Project of Hainan Provincial Department of Education(No.Hnky2022-38)Innovation and Entrepreneurship Training Program for College Students of Hainan Medical College(No.S202211810034)。
文摘Objective:The aim of this study is to investigate the effects of Hepatocyte Growth Factor(HGF)on the expression levels of IL-8,TNF-α,IL-4,and IL-21 in mice with liver injury induced by CCL_(4).Methods:An acute liver injury mouse model was established using CCL_(4),and hepatocytes and white blood cells were separated by gradient density centrifugation.Different concentrations of HGF were added in vitro,and the expression levels of cytokines were detected using ELISA.Results:In the in vivo injury model,the hepatocyte experiment results showed that the expression level of IL-8 was reduced in the 10 ng/mL HGF group compared to the injured hepatocyte group(P<0.05),and increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.05).For IL-4,the expression levels were reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the injured hepatocyte group.The white blood cell experiment results showed that the expression levels of TNF-αwere reduced in both the 10ng/ml HGF group(P<0.05)and the 25 ng/mL HGF group(P<0.05)compared to the injured white blood cell group.In the in vitro injury model,hepatocyte experiment results showed that the expression levels of TNF-αwere reduced in both the 25 ng/mL HGF group(P<0.05)and the 50 ng/mL HGF group(P<0.05)compared to the normal control group.For IL-4,the expression level was reduced in the 25 ng/mL HGF group compared to the normal control group(P<0.05).The white blood cell experiment results showed that the expression level of TNF-αwas increased in the 50 ng/mL HGF group compared to the 10 ng/mL HGF group(P<0.001);for IL-21,the expression levels were reduced in the CCL_(4) model group(P<0.05),10 ng/mL HGF group(P<0.05),25 ng/mL HGF group(P<0.05),and 50 ng/mL HGF group(P<0.05)compared to the normal control group.Conclusion:when the liver of mice is acutely damaged by CCL_(4),HGF can reduce the expression levels of inflammatory cytokines IL-8,TNF-α,IL-4 in hepatocytes,and TNF-αin liver white blood cells.
基金the Innovation Project of Jilin Academy of Agricultural Sciences(CXGC2017ZY011)Major Project of Jilin Provincial Department of Science and Technology(20170204046NY)。
文摘[Objectives]To explore the protective effects of flavonoids from Pteridium aquilinum(PAFL)on carbon tetracholoride(CCl_(4))-induced acute liver injury in mice and its potential mechanism.[Methods]All mice were randomly divided into four groups(n=10 in each),normal group,CCl_(4)group,CCl_(4)+PAFL groups[treated with PAFL(50 or 200 mg/kg)].Animal treatment was continued for 7 consecutive days.The blood was collected after injection of CCl_(4)for 24 h,and the liver tissue was removed from the mice and stored at-80℃.[Results]The PAFL(50 and 200 mg/kg)significantly inhibited the increase of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)levels in serum caused by CCl_(4)treatment.PAFL administration not only increased the activity of antioxidant enzymes superoxide dismutase(SOD),Glutathione(GSH)and catalase(CAT)in mice,but also reduced the level of malondialdehyde(MDA).Meanwhile,PAFL administration decreased the expression of nuclear factor-kappa B(NF-κB)and Cyclooxygenase-2(COX-2)proteins and inhibited the release of pro-inflammatory factors tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin 6(IL-6).In addition,PAFL(200 mg/kg)treatment down-regulated extracellular regulated protein kinases(ERK)and c-Jun N-terminal kinase(JNK)protein levels in liver tissue.[Conclusions]These findings clearly indicate that the protective effects of PAFL on CCl_(4)-induced acute liver injury is related to its antioxidant and anti-inflammatory activity,which may be mediated by NF-κB and MAPKs signaling pathways.
基金Natural Science Foundation of the Anhui Higher Education Institutions of China(Grant No.KJ2019A0166)the National Natural Science Foundation of China(Grant No.31772786)。
文摘研究黄精(Polygonatumsibiricum,PS)对CCl_(4)诱导的大鼠肝损伤的保护作用及其抗氧化机制。采用一次性腹腔注射50%四氯化碳油溶液建立大鼠急性肝损伤模型,用黄精水提物(PSAE)灌胃治疗,水飞蓟素作为阳性对照药物,连续7天。PSAE显著降低了血清丙氨酸转氨酶、天冬氨酸转氨酶和碱性磷酸酶(AST、ALT和ALP)的水平(P<0.05),增加了肝组织谷胱甘肽(GSH)和超氧化物歧化酶(T-SOD)的水平(P<0.05),降低了肝组织中丙二醛的活性(P<0.05),并显著降低了肝细胞中的活性氧水平(P<0.05)。在肝组织中,核因子类红细胞2相关因子2(Nrf2),NAD(P)H醌脱氢酶1(NQO-1),血红素加氧酶1(HO-1)mRNA的表达水平显著升高,p53 mRNA表达显著降低(P<0.05),Bcl-2(P<0.05)和Bcl-x L mRNA的表达升高,HO-1蛋白表达升高,Keap-1 mRNA表达无明显差异(P>0.05)。因此,黄精对CCl_(4)诱导的急性肝损伤有较好的保护作用,其机制与有效调节Nrf2-Keap1-ARE通路相关基因和蛋白质的表达、抑制p53途径介导的肝细胞凋亡有关。
