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目的探讨甘草次酸衍生物(TY501)对四氯化碳(CCl_4)致小鼠肝纤维化的保护作用及其机制。方法采用经典CCl_4造模法建立小鼠肝纤维化模型,给予高、中、低剂量(45、15、5 mg/kg)TY501干预治疗,用秋水仙碱(0.36 mg/kg)作阳性对照。给药30 d后,检测各组小鼠肝功能指标、肝纤维化指标、肝组织羟脯氨酸(Hyp)和转化生长因子-β1(TGF-β1)的量,并取其肝组织进行病理学染色。结果与模型组相比,TY501各治疗组肝功能指标(ALT、AST、ALP、ALB)、肝纤维化指标(HA、LN、PCIII、CIV)及肝组织Hyp、TGF-β1的量均有不同程度改善,其中高剂量组改善作用最为明显(P<0.05、0.01);肝组织病理学切片显示,给药组小鼠肝纤维化程度降低,有逆转趋势。结论 TY501对CCl_4造成的肝纤维化有明显的保护作用。
Objective To investigate the protective effect and its mechanism of glycyrrhetinic acid derivative (TY501) on hepatic fibrosis induced by carbon tetrachloride (CCl_4) in mice. Methods The mouse model of hepatic fibrosis was induced by classical CCl_4 modeling. TY501 (45, 15, and 5 mg / kg) was administered to mice with liver injury. Colchicine (0.36 mg / kg) was used as the positive control. After administration for 30 days, the indexes of hepatic function, indexes of hepatic fibrosis, Hyp and TGF-β1 in liver tissues of mice were detected, Neo-Confucianism Results Compared with the model group, the liver function indexes (ALT, AST, ALP, ALB), liver fibrosis indexes (HA, LN, PCIII and CIV) and Hyp and TGF- (P <0.05, 0.01). The histopathological sections of liver showed that the degree of hepatic fibrosis was decreased and the tendency was reversed. Conclusion TY501 has obvious protective effect on hepatic fibrosis induced by CCl_4.