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目的:观察干扰素α-2a(interferon alfa-2a,IFNα-2a)对CCl4诱导肝纤维化的作用及影响因素.方法:建立CCl4诱导大鼠肝纤维化模型,SD雌性大鼠50只,分成5组,每组10只,即生理盐水对照组(A组)、纤维化模型组(B组)、6×104U/kgIFNα-2a干预组(C组)、12×104U/kgIFNα-2a干预组(D组)及6×104U/kgIFNα-2a对照组(E组).造模8wk时采集血标本及肝组织标本,分别进行肝功能指标ALT、AST、TBIL、TP,肝纤维化指标HA、LN、PCIII检测,及组织病理形态学观察包括HE染色、Masson染色和网状纤维染色.结果:CCl4腹腔注射成功诱导大鼠肝纤维化模型,表现为汇管区周围纤维化明显,有芒状纤维和纤维间隔形成.血清学检测:B、C、D组ALT、AST、TBiL、HA、LN均明显高于A组(F值分别为14.8,4.4,7.8,51.3,68.9;均P<0.05);C、D组ALT、AST、TBiL均明显低于B组;D组的上述指标又明显低于C组.组织病理:HE染色、Masson染色和网状纤维染色均显示,C、D组肝组织炎症及肝纤维化程度较B组显著减轻,D组较C组肝纤维化程度更轻,A、E组肝组织未见炎症及纤维化.结论:IFNα-2a能够阻断CCl4诱导肝纤维化,其作用效果随IFNα-2a剂量增加而增强.
Objective: To observe the effects of interferon alfa-2a (IFNα-2a) on CCl4-induced hepatic fibrosis and its influencing factors.Methods: Fifty SD female rats with CCl4-induced hepatic fibrosis were divided into 5 groups, 10 rats in each group, namely saline control group (group A), fibrosis model group (group B), 6 × 104U / kg IFNα-2a intervention group (group C) and 12 × 104U / kg IFNα-2a intervention group (Group D) and 6 × 104U / kg IFNα-2a control group (group E). Blood samples and liver tissue samples were collected at 8 weeks after model establishment and liver function indexes such as ALT, AST, TBIL, TP, LN, PCIII and histopathological examination including HE staining, Masson staining and reticular fiber staining.Results: The rat model of hepatic fibrosis induced by CCl4 was successfully induced by intraperitoneal injection of CCl4, with obvious fibrosis around the portal area, And fibrin septa.The results of serological tests showed that ALT, AST, TBiL, HA and LN in group B, C and D were significantly higher than those in group A (F = 14.8,4.4,7.8,51.3,68.9, all P <0.05) ; The ALT, AST and TBiL in group C and D were significantly lower than those in group B, and the above indexes in group D were significantly lower than those in group C. Histopathology: HE staining, Masson staining and reticular fiber staining showed that group C and D The degree of inflammation and hepatic fibrosis was significantly lower than that of group B, the degree of liver fibrosis was lighter in group D than in group C, and no inflammation and fibrosis in group A and group E. Conclusion IFNα-2a can block CCl4-induced hepatic fibrosis The effect of IFNα-2a increased with the dose.