α-2a干扰素对大鼠肝组织bcl-2基因表达的影响及意义

Effects of IFNα-2a on bcl-2 expression in the f ibrotic liver of rats

目的:探讨α-2a干扰素(IFNα-2a)对大鼠肝组织bcl-2基因表达的影响和对肝纤维化的作用及其机制.方法:将SD大鼠随机分成纤维化模型组(A组,CCl4诱导形成大鼠肝纤维化模型),对照组(B组)及IFNα-2a干预组(C组).用RT-PCR法检测各组大鼠肝脏bcl-2的表达,常规HE和网状纤维染色检测肝组织标本.结果:C组纤维化程度及肝细胞脂肪变性较A组显著减轻,但肝组织炎症改变无显著差异性.C组bcl-2基因蛋白表达显著低于A组(P<0.01),但显著高于B组bcl-2基因蛋白表达的量(P<0.01).结论:IFNα-2a能够阻断CCl4诱导的肝纤维化和减少肝脂肪变性.其机制与bcl-2基因表达有关,可能通过调节bcl-2基因表达与HSC凋亡,从而阻断肝纤维化和减少肝脂肪变性.

AIM： To investigate the effects of interferon α-2a （IFNα-2a） on bcl-2 gene expression in the f ibrotic liver of rats and explore potential mechanisms involved. METHODS： Hepatic f ibrosis was induced in rats by subcutaneous injection of carbon tetrachloride （CCl4）. Sprague-Dawley rats were randomly divided into normal control group, f ibrosis mod-el group and IFNα-2a intervention group. The expression of bcl-2 gene in the liver was detected by reverse transcription-polymerase chain reaction （RT-PCR）. Liver tissue samples were taken for conventional hematoxylin and eosin （HE） staining and reticular fiber staining to observe histological changes. RESULTS： A rat model of liver fibrosis was successfully established. IFNα-2a treatment signifi cantly ameliorated liver f ibrosis and fatty degeneration, but showed no impact on hepatic inflammation in fibrotic rats. The expression level of bcl-2 mRNA in the IFNα-2a intervention group was significantly lower than that in the fi brosis model group （P 〈 0.01）, but higher than that in the normal control group （P 〈 0.01）. CONCLUSION： IFNα-2a can effectively amelio- rate CCl4-induced hepatic fi brosis and liver fatty degeneration possibly via a mechanism associated with downregulating bcl-2 gene expression and controlling apoptosis of HSC.