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目的:探究复方银杏叶制剂(CGB)对非酒精性脂肪肝(NAFLD)的干预作用机制。方法:采用高脂饮食诱导C57BL/6小鼠NAFLD模型,于造模第2周起以600,200 mg·kg~(-1)·d~(-1)的CGB灌胃8周,观察小鼠血清生化指标谷丙转氨酶(ALT)、谷草转氨酶(AST)、甘油三酯(TG)、胆固醇(CHOL)、血清内毒素(LPS)水平、肝组织病理变化与肝脏TNF-α表达;电镜观察小肠上皮细胞紧密连接变化,测定ZO-1,Occludin,Claudin-1紧密连接蛋白表达。结果:与正常组比较,模型组小鼠肝脏发生明显脂肪变性,TNF-α表达显著增高(P<0.01);血清ALT,AST,TG,CHOL与LPS水平均显著增高(P<0.01,P<0.05);肠上皮紧密连接结构受损,ZO-1,Occludin,Claudin-1表达显著降低(P<0.01)。与模型组比较,CGB高、低剂量组明显减轻肝组织脂肪变性,TNF-α表达显著降低(P<0.01,P<0.05);血清AST,TG,CHOL与LPS水平均显著降低(P<0.01,P<0.05);肠道紧密连接破坏程度减轻,ZO-1,Occludin表达显著增高(P<0.05)。结论:CGB可以保护肠道紧密连接,减少LPS肠渗漏,缓解肝脏脂肪变性和炎症,防治NAFLD的发生发展。
Objective: To investigate the mechanism of intervention of Compound Ginkgo Biloba (GGB) on Non-alcoholic Fatty Liver (NAFLD). Methods: The NAFLD model of C57BL / 6 mice was induced by high fat diet, and the mice were inoculated with CGB 600,200 mg · kg -1 · d -1 for 8 weeks from the second week of model making. Biochemical indicators ALT, AST, CHOL, LPS, hepatic histopathological changes and hepatic TNF-αexpression were observed by electron microscopy. Tight junctional changes in cells, determination of ZO-1, Occludin, Claudin-1 tight junction protein expression. Results: Compared with the normal group, the hepatic steatosis and the expression of TNF-α in the model group were significantly increased (P <0.01), and the levels of serum ALT, AST, TG, CHOL and LPS were significantly increased (P < 0.05). The structure of intestinal tight junction was impaired, and the expressions of ZO-1, Occludin and Claudin-1 were significantly decreased (P <0.01). The levels of AST, TG, CHOL and LPS in serum of CGB high and low dose groups were significantly lower than those of model group (P <0.01, P <0.05) , P <0.05). The extent of intestinal tight junctions was relieved and the expression of ZO-1 and Occludin were significantly increased (P <0.05). Conclusion: CGB can protect intestinal tight junctions, reduce intestinal leakage of LPS, alleviate hepatic steatosis and inflammation and prevent the occurrence and development of NAFLD.