荔枝核总黄酮对肝纤维化大鼠肝组织MMP-2表达的影响

目的:观察基质金属酶-2(MM P-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.

Effect of Total Flavone from Litchi chinensis Sonn on Expression of MMP-2 in Rats Livers with Hepatic Fibrosis

Objective: To observe theexpression of matrix metalloproteinase-2 (MMP-2) in the livers of rats with hepatic fibrosis, and the effects of total flavone from Litchi chinensis Sonn (TFL) on rats. Method: The rat model of hepatic fibrosis was established by intraperitoneal injection of DMN(dimethylnitrosamine). TFL was orally given at a dose of 100, 200 mg·kg^-1·d^-1. Colchicine was used as a positive control. After 6 weeks, all rats were sacrificed and their left liver lobes were examined histopathologically. The degree of fibrosis was evaluated by HE and Masson straining; serum levels of alanine transaminase (ALT) and aspartate aminotransferase(AST) were detected by an biochemical analytical tool in the laboratory test department of our hospital. The expression of MMP-2 in liver tissue was assessed by S-P immunohistochemical staining using polyclonal antibodies against MMP-2. Result: Serum levels of ALT nad AST were significantly lower in the TFL group and the colchicine group than that in the fibrosis model group (all P<0.05). The degree of hepatic fibrosis in the TFL group was less severe compared with those of the fibrosis model. The expression levels of MMP-2 in the TFL group and colchicine group were lower than in that the liver fibrosis model group (P<0.05). Conclusion: TEL can improve the degree of fibrosis,the mechanism possibly involve the inhibition of the expression of MMP-2.