5,2',4'-三羟基-6,7,5'-三甲氧基黄酮通过内质网应激反应对CCl_4所致大鼠肝纤维化的保护作用  

Protective effect of 5,2',4'-trihydroxy-6,7,5'-trimethoxyflavonethrough endoplasmic reticulum stress in the process of CCl_4 induced liver fibrosis in rats

作　　者：房岩[1] 蔡牧辰 张学武[1] 

机构地区：[1]延边大学医学院,吉林延吉133000

出　　处：《时珍国医国药》2015年第4期838-840,共3页Lishizhen Medicine and Materia Medica Research

基　　金：国家自然科学基金(No.81260655)

摘　　要：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 study the protective effect of 5,2＇,4＇- trihydroxy - 6,7,5＇- trimethoxyflavone in the process of CCI4 induced liver fibrosis in rats. Methods 72 rats were randomly divided into 6 groups ：control , model, Col,5 μmol TTF1,10 μmol TFF1,20 μmol TTF1 ,and 12 rats in each group. The microscopic changes of rats＇liver were investigated in the process of liver fi- brosis, and the changes in endoplasmic reticulum stress - related factors were detected by western blot. Results HE Staining showed that the model group liver cells had broader spotty necrosis, with inflammatory cell infiltration, and periportal tissue was proliferated obviously ,fibrosis grading up to grade Ⅲ ;Col and TTF1 groups were much better than model group, and fibrosis grad- ing up to grade. The changes on endoplasmic reticulum stress - related factors were detected by western blot that GRP78, PERK, IRE1α,ATF6 and Caspase -12 were decreased significantly compared with model group. Conclusion TTF1 shows a protective effect in the process of CCl4 induced liver fibrosis in rats, and the inhibition of endoplasmic reticulum stress pathway may be one of the main mechanisms.

关 键 词：5 2' 4'-三羟基-6 7 5'-三甲氧基黄酮 大鼠 内质网应激 肝纤维化 

分 类 号：R285.5[医药卫生—中药学]