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目的 观察干扰素 α 2a(IFN α 2a)对实验性肝纤维化时肝脏组织学及血清肝纤维化指标的影响。方法 利用免疫组织化学、放射免疫技术及MV1LU细胞生长抑制法 ,对CCl4诱导大鼠肝纤维化不同阶段肝脏组织学及透明质酸 (HA)、层黏蛋白 (LN)、Ⅳ胶原 (ⅣC)及转化生长因子 β(TGF β)的变化进行了观察。 结果 在肝纤维化早期 (3周 ) ,干扰素 α治疗组肝脏炎症计分、纤维化计分及血清纤维化指标与模型对照组比较差异无显著性 (P >0 .0 5 )。在肝纤维化中期 (6周 )及晚期(12周 ) ,IFN α 2a治疗组组织学肝脏炎症计分、纤维化计分与模型对照组对比差异有显著性 (P <0 .0 5及 <0 .0 1)。血清TGF β与HA、LN、ⅣC呈正相关 ,TGF β活性与肝纤维化动态变化相一致。 结论 干扰素 α 2a可明显减轻肝脏炎症 ,减少或逆转肝纤维化的作用 ,其机制与抑制肝脏中TGF β的活性有关。
Objective To observe the effects of interferon α 2a (IFN α 2a) on liver histology and serum hepatic fibrosis in experimental liver fibrosis. Methods Immunohistochemistry, radioimmunoassay and MV1LU cell growth inhibition were used to evaluate the effects of CCl4 on the histopathology, histological changes of hyaluronic acid (HA), laminin (LN), collagen Ⅳ (ⅣC) Transforming growth factor β (TGF β) changes were observed. Results In the early stage of hepatic fibrosis (3 weeks), there was no significant difference in liver inflammation score, fibrosis score and serum fibrosis between the model group and the interferon α group (P> 0.05). Liver fibrosis in the middle (6 weeks) and late (12 weeks), IFN α 2a treatment group histological liver inflammation score, fibrosis score and the model control group, the difference was significant (P <0.05 and < 0 .0 1). Serum TGFβ was positively correlated with HA, LN, ⅣC, TGFβ activity was consistent with the dynamic changes of liver fibrosis. Conclusions Interferon α 2a can significantly reduce hepatic inflammation and reduce or reverse the effect of hepatic fibrosis. Its mechanism is related to the inhibition of TGF β activity in the liver.