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目的探讨5,2’,4’-三羟基-6,7,5’-三甲氧基黄酮(TTF1)通过内质网应激(ERS)对二乙基亚硝胺(DEN)诱发大鼠肝脏癌前病变过程的保护作用。方法 60只Wistar大鼠随机分为5组:正常组、模型组和TTF1给药组(5,10,20μmol/kg),每组12只,利用改良的Solt-Farber氏方法建立大鼠肝癌前病变模型;光镜检测大鼠肝脏变化及免疫组织化学方法检测大鼠肝脏GST-P的表达;免疫印迹法检测ERS相关因子的变化。结果光镜结果显示,模型组肝细胞结构异常,排列失常,汇管区小细胞、纤维组织增生散在变性细胞,嗜碱性肝细胞和玻璃样的透明肝细胞灶混合排列拥挤形成的肝细胞增生性结节,TTF1给药组肝细胞变化轻于模型组;与模型组比较,TTF1给药组大鼠肝组织GST-P表达明显低于模型组,GRP78,PERK,IRE1α,ATF6和Caspase12大量活化表达。结论 TTF1对大鼠肝脏癌前病变有抑制作用,抑制ERS可能是作用机制之一。
Objective To investigate the effects of 5,2 ’, 4’-trihydroxy-6,7,5’-trimethoxyflavone (TTF1) on the liver of rat induced by diethylnitrosamine (DEN) via endoplasmic reticulum stress (ERS) Protective effect of precancerous lesions. Methods Sixty Wistar rats were randomly divided into five groups: normal group, model group and TTF1 group (5, 10 and 20μmol / kg), with 12 rats in each group. Solvent-Farber’s The pathological changes were observed by light microscopy. The expression of GST-P in rat liver was detected by light microscopy and the expression of ERS was detected by immunoblotting. Results The results of light microscopy showed that the hepatocytes in the model group were abnormally arranged and arranged abnormally. The small cells in the portal area and the proliferation of fibrous tissue were scattered in the degenerated cells. The basophilic hepatocytes and the glass-like transparent hepatocytes were crowded to form hepatic cell proliferation Compared with the model group, the expression of GST-P in the liver tissue of TTF1-treated group was significantly lower than that of the model group, with significant activation of GRP78, PERK, IRE1α, ATF6 and Caspase12 . Conclusion TTF1 can inhibit the precancerous lesion of liver in rats, and inhibition of ERS may be one of the mechanisms.