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目的探讨蛇毒血凝酶如何调控TGF-β1/Smads信号通路从而干预肝纤维化的发生发展。方法选取健康清洁级SD雄性大鼠60只,随机分为正常组、模型组和蛇毒血凝酶实验组各20只。模型组和实验组用皮下注射CCl4诱导肝纤维化大鼠模型为评价载体,正常组皮下注射花生油作为对照,检测血清中ALT、AST、ALB含量和Col-IV、LN参数,苏木素-伊红(HE)染色测定肝纤维化程度表达,用RT-PCR法检测肝组织中TGF-β1及Smad3水平,Western blot法测定肝组织TGF-β1及Smad3蛋白表达。结果实验组的HE染色显示肝纤维化程度好转。正常组和实验组的血清ALT、AST和ALB含量明显低于模型组大鼠(P<0.05),实验组与正常组比较,血清ALT、AST和ALB含量差异无统计学意义(P>0.05)。模型组大鼠血清TCol-IV、LN参数明显高于正常组和实验组(P<0.05);实验组与正常组相比差异无统计学意义(P>0.05)。实验组与正常组比较,大鼠肝脏组织TGF-β1和Smad3的表达无明显差异(P>0.05);实验组TGF-β1和Smad3的表达高于正常组和模型组(P<0.05)。与模型组相比,正常组和实验组TGF-β1及Smad3蛋白表达明显降低(P<0.05);实验组与正常组比较,TGF-β1及Smad3蛋白表达差异无统计学意义(P>0.05)。结论蛇毒血凝酶干预能显著改善肝功能,降低肝纤维化程度,提示其作用机制可能与调控肝组织TGF-β1/Smads信号通路有关。
Objective To investigate how snake venom hemagglutinin can regulate the TGF-β1 / Smads signaling pathway and thus interfere with the development of hepatic fibrosis. Methods Sixty male SD rats were randomly divided into normal group, model group and venom hemagglutinin experimental group (n = 20). The rats in model group and experimental group were subcutaneously injected with CCl4 to induce hepatic fibrosis. The rats in normal group were injected subcutaneously with peanut oil as control. The content of ALT, AST and ALB in serum and the parameters of Col-IV, LN, hematoxylin-eosin HE staining was used to detect the expression of TGF-β1 and Smad3 in liver tissue. RT-PCR was used to detect the expression of TGF-β1 and Smad3 in liver tissue. Western blot was used to detect the expression of TGF-β1 and Smad3. Results HE staining of the experimental group showed that the degree of liver fibrosis improved. The levels of serum ALT, AST and ALB in normal group and experimental group were significantly lower than those in model group (P <0.05). There was no significant difference in serum ALT, AST and ALB between experimental group and normal group (P> 0.05) . The serum TCol-IV and LN parameters in the model group were significantly higher than those in the normal group and the experimental group (P <0.05). There was no significant difference between the experimental group and the normal group (P> 0.05). Compared with normal group, the expression of TGF-β1 and Smad3 in experimental group had no significant difference (P> 0.05). The expression of TGF-β1 and Smad3 in experimental group was higher than that in normal group and model group (P <0.05). Compared with the model group, the expression of TGF-β1 and Smad3 in the normal group and experimental group were significantly decreased (P <0.05); there was no significant difference in the expression of TGF-β1 and Smad3 between the experimental group and the normal group (P> 0.05) . Conclusion Snake venom hemagglutinin treatment can significantly improve liver function and reduce the degree of liver fibrosis, suggesting that its mechanism of action may be related to the regulation of liver TGF-β1 / Smads signaling pathway.