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目的:观察基质金属酶-2(MMP-2)在实验性肝纤维化大鼠组织中的表达,探讨荔枝核总黄酮(total flavone from Litchi chinensis Sonn,TFL)抗肝纤维化的作用机制。方法:大鼠随机分为正常组,模型组,TFL高,低剂量组及秋水仙碱阳性对照组。模型组,TFL治疗组及秋水仙碱阳性对照组以二甲基亚硝胺腹腔注射4周制作大鼠肝纤维化模型;造模同时TFL高、低剂量组及秋水仙碱分别以TFL(200,100 mg·kg-1·d-1),秋水仙碱(colchicine,col)灌胃给药,正常组及模型组给予等体积生理盐水灌胃,6周后处死大鼠,抽取下腔静脉血检测谷草转氨酶(AST),谷丙转氨酶(ALT),取肝脏同一部位行HE,Masson染色观察大鼠肝纤维化程度,采用免疫组化检测各组肝组织MMP-2的表达。结果:TFL高、低剂量组和正常组血清AST,ALT均明显低于模型组,具有显著性差异(P<0.05)。与模型组比较TFL治疗组可明显抑制MMP-2的表达(P<0.05),改善大鼠肝纤维化程度(P<0.05)。结论:荔枝核总黄酮可减轻肝损伤及改善实验性大鼠肝纤维化程度,抑制MMP-2的表达可能是其抗肝纤维化作用的机制之一。
OBJECTIVE: To investigate the expression of matrix metalloproteinase-2 (MMP-2) in experimental hepatic fibrosis rats and to explore the mechanism of total flavone from Litchi chinensis Sonn (TFL) against hepatic fibrosis. Methods: The rats were randomly divided into normal group, model group, TFL high and low dose groups and colchicine positive control group. Model group, TFL treatment group and colchicine positive control group were injected with dimethylnitrosamine for 4 weeks to make rat model of hepatic fibrosis; while the models of TFL high and low dose group and colchicine were respectively treated with TFL (200,100 mg · kg-1 · d-1) and colchicine (col) were intragastrically administrated. The rats in the normal group and model group were given the same volume of normal saline for gavage. After 6 weeks, the rats were killed and the inferior vena cava blood was collected Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were determined. The same part of the liver was taken for HE and Masson staining to observe the degree of hepatic fibrosis. The expression of MMP-2 in each group was detected by immunohistochemistry. Results: The levels of serum AST and ALT in high and low TFL group and normal group were significantly lower than those in model group (P <0.05). Compared with the model group, TFL treatment group could significantly inhibit the expression of MMP-2 (P <0.05) and improve the degree of hepatic fibrosis in rats (P <0.05). Conclusion: The total flavonoids of litchi nucleus can reduce liver injury and improve the degree of hepatic fibrosis in experimental rats. Inhibition of MMP-2 expression may be one of its mechanisms of anti-hepatic fibrosis.