摘要
熊果酸和齐墩果酸的抗氧化作用能对抗各种原因引起的氧化应激所致的肝组织脂质过氧化反应、炎性损伤、脂肪变和纤维化。熊果酸和齐墩果酸通过阻断两面神激酶2-信号传导及转录激活因子3(JAK2-STAT3)信号转导,抑制还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶(NOX)活化,阻止静息态肝星状细胞活化、增殖,促进活化态肝星状细胞凋亡,从而减少胶原生成、增加细胞外基质降解,产生防治肝纤维化的作用。熊果酸和齐墩果酸诱导肝脏去毒酶和外排转运体表达,降低胆汁淤积动物血清胆汁酸、胆红素水平和肝脏胆汁酸水平,减轻胆汁淤积性肝损伤和纤维化;还可通过降血脂作用抑制肝外脂质在肝脏沉积、抑制肝脏脂质生物合成和促进脂质代谢,阻滞肝脂肪变的发生和发展。
Anti-oxidation of ursolic acid and oleanolic acid antagonizes oxidative stress-induced lipid peroxidation, inflammatory injury, steatosis, and fibrosis in liver tissue. Ursolic acid and oleanolic acid could block static state hepatic stellate cells activation and proliferation, and promote active state hepatic stellate cells apoptosis, thus decrease expression of collagen, and increase decomposition of extracellular matrix, to produce the effect in prevention and treatment of hepatic fibrosis by obstruction of JAK2-STAT3 signal transduction to inhibit NOX activation. Ursolic acid and oleanolic acid induce expression of detoxification enzymes and efflux transporters to reduce serum levels of bile acids and bilirubin, and liver levels of bile acids in cholestatic animal, thus ameliorating cholestatic liver injury and fibrosis. Ursolic acid and oleanolic acid inhibit occurrence and development of hepatic steatosis via decreasing hyperlipidemia to inhibit lipid out of liver accumulating to liver, inhibiting hepatic lipid synthesis, and improving lipid metabolism.
出处
《药物评价研究》
CAS
2017年第2期270-278,共9页
Drug Evaluation Research
关键词
熊果酸
齐墩果酸
肝脂肪变
肝纤维化
作用机制
ursolic acid
oleanolic acid
liver steatosis
liver fibrosis
mechanism
