抗纤维化因子在肝硬化进程中动态变化的研究

目的 深入探讨肠源性内毒素血症所诱发的细胞因子IL－10在肝纤维化发生发展中的作用机制。方法 采用本室建立的以复合因子致肝纤维化、肝硬化动物模型进行实验。对血浆IL－10水平进行动态观察。结果 肝硬化形成进程中血浆内毒素水平与肝组织胶原蛋白含量均渐进性升高，血浆白细胞介素10（IL－10）在第5周前随肝纤维化进程逐渐增高，待至第5周开始IL－10逐渐下降，到第8周末降至最低。肝组织学观察结果显示，第4周末肝组织中每100个肝细胞中含淋巴细胞数明显高于第8周末。结论 肝纤维化的发生、发展与肠源性内毒素血症密切相关。随着肝内炎症反应的消退，IL－10已不再发挥其抗纤维化作用，故肝纤维化程度进一步加剧。

Dynamic changes of interleukin-10 at differe nt stages of hepatic cirrhosis

Objective To inquire further into the mechanism of cytokine IL 10 induced by intestinal endotoxemia in the development of hepatic fibrosis. Methods The hepatic fibrosis and cirrhosis rat models were made by carbon tetrachloride (CCl 4) and dietetic factor.The plasma IL 10 levels were observed kinetically. Results With the liver fibrosis developing plasma endotoxin level and hepatic collagen contents both increased progressively,the plasma IL 10 tended to increase before 4th week and increased to peak,but IL 10 tended to reduce from 5th week and reduced to miximum at the 8th week. Histopathologic HE stain showed that the number of lymphocyte in hepatic tissue at 4th week were much more than at 8th week. Conclusion The hepatic fibrosis is associated closely with intestinal endotoxemia.Along with weakening of the inflammatory reaction in liver,IL 10 no more plays an anti fibrosis effect further, so the hepatic fibrosis process becomes more serious.