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目的探讨5,2’,4’-三羟基-6,7,5’-三甲氧基黄酮(TTF1)对四氯化碳(CCl4)所致大鼠肝纤维化的保护作用。方法72只大鼠随机分为6组:正常组、模型组、秋水仙碱(colchicine,Col)组和TTF1给药组(5,10,20μmol/kg),每组12只。观察TTF1对CCl4所致慢性肝损伤病理学变化,免疫印迹法检测内质网应激(endoplasmic reticulum stress,ERS)相关因子表达。结果病理学检查结果显示,模型组肝细胞有较广泛的点状坏死,伴炎症细胞浸润,肝细胞增生较为明显,汇管区结缔组织增生,肝纤维化分级的Ⅲ级;Col组和TTF1给药组变化类似:肝细胞点状坏死及炎症细胞浸润轻于模型组,肝纤维化分级为Ⅰ级。与模型组比较,Col组和TTF1给药组大鼠肝组织的GRP78,PERK,IRE1α,ATF6和Caspase-12表达明显降低。结论 TTF1对CCl4所致大鼠肝纤维化有一定的保护作用,抑制ERS反应可能是其主要作用机制之一。
Objective To investigate the protective effect of 5,2 ’, 4’-trihydroxy-6,7,5’-trimethoxyflavone (TTF1) on liver fibrosis induced by carbon tetrachloride (CCl4) in rats. Methods 72 rats were randomly divided into 6 groups: normal group, model group, colchicine (Col) group and TTF1 group (5, 10, 20μmol / kg) The pathological changes of TTF1 on CCl4-induced chronic liver injury were observed, and the expressions of endoplasmic reticulum stress (ERS) related factors were detected by Western blotting. Results The results of pathological examination showed that the hepatocytes in model group had more extensive punctate necrosis with infiltration of inflammatory cells and hepatocyte hyperplasia, connective tissue hyperplasia and hepatic fibrosis grade Ⅲ in colorectal area, and Col group and TTF1 Group changes similar to: hepatocytes punctate necrosis and inflammatory cell infiltration was lighter than the model group, liver fibrosis grade Ⅰ. Compared with the model group, the expressions of GRP78, PERK, IRE1α, ATF6 and Caspase-12 in the liver tissue of Col group and TTF1 group were significantly decreased. Conclusion TTF1 may protect CCl4-induced hepatic fibrosis in rats and inhibition of ERS may be one of its main mechanisms.