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[目的]研究吡喹酮杀虫治疗和γ-干扰素(IFN-γ)抗肝纤维化治疗对日本血吸虫性肝纤维化小鼠体内Smads分子的影响。[方法]日本血吸虫尾蚴感染BALB/c小鼠16周后形成肝纤维化动物模型,随机分成3组:0.85%氯化钠组、吡喹酮组和吡喹酮联合IFN-γ(联合)组,并以10只正常BALB/c小鼠作为正常对照。治疗8周后取小鼠肝组织,进行肝组织病理学检查,观察肝纤维化程度;应用RT-PCR法检测肝组织中Smad2、Smad3、Smad4、Smad7和IFN-γmRNA水平。[结果]吡喹酮组治疗后,肝纤维化程度、Smad2 mRNA水平与0.85%氯化钠组比较差异无统计学意义,Smad3 mRNA水平下降到正常,IFN-γmRNA水平明显增高。联合组治疗后,肝纤维化程度明显减轻,但尚未达到正常水平,Smad2 mRNA水平仍低于正常水平,Smad3和Smad7 mRNA水平上调,IFN-γmRNA处于正常水平。[结论]吡喹酮联合IFN-γ抗纤维化的机制是促进Smad7的表达,但Smad2 mRNA的下调,Smad3 mRNA的上调可能导致联合治疗未能使肝纤维化完全逆转。
[Objective] To study the effect of praziquantel insecticide treatment and γ-interferon (IFN-γ) anti-hepatic fibrosis therapy on Smads molecules in schistosomiasis japonicus mice. [Method] BALB / c mice were infected with cercariae of Schistosoma japonicum 16 weeks later to form animal models of hepatic fibrosis and were randomly divided into three groups: 0.85% sodium chloride group, praziquantel group and praziquantel combined with IFN-γ group , And 10 normal BALB / c mice as normal control. After 8 weeks of treatment, the liver tissues of the mice were taken for liver histopathological examination to observe the degree of hepatic fibrosis. The levels of Smad2, Smad3, Smad4, Smad7 and IFN-γmRNA were detected by RT-PCR. [Results] After treatment with praziquantel, there was no significant difference in the degree of liver fibrosis, Smad2 mRNA level compared with 0.85% sodium chloride group, the Smad3 mRNA level decreased to normal, and the level of IFN-γmRNA increased significantly. After the combination therapy, the degree of hepatic fibrosis was significantly reduced, but not yet reached the normal level. The level of Smad2 mRNA was still below the normal level, the level of Smad3 and Smad7 mRNA was up-regulated, and the level of IFN-γ mRNA was normal. [Conclusion] The mechanism of praziquantel combined with IFN-γ anti-fibrosis is to promote the expression of Smad7. However, down-regulation of Smad2 mRNA and up-regulation of Smad3 mRNA may lead to complete reversal of hepatic fibrosis by combination therapy.