摘要
目的:利用CCl4诱导肝纤维化动物实验模型,研究甘草酸治疗前后smad7的变化,揭示甘草酸抗肝纤维化的分子生物学机制。方法:将89只雄性大鼠随机分成3组:正常对照组24只;CCl4组33只;甘草酸治疗组32只。其中甘草酸治疗组腹腔注射0.2%的甘草酸氨水溶液,每周3次。应用免疫组织化学法检测不同时期(1、2、4、8周)3组大鼠Smad7的表达。结果:研究发现甘草酸在肝纤维化发生的各个阶段均能改善肝脏的病理变化,且其作用在肝纤维化的后期更为明显。在甘草酸治疗组中Smad7的表达在第4周明显超过CCl4组。结论:甘草酸能改善CCl4诱导肝纤维化大鼠的病理变化。甘草酸抑制肝纤维化的作用机制之一是通过增强Smad7的表达实现的。
Objective: To investigate the effects of glycyrrhizin on smad signal pathway in CCL induced rat liver fibrosis and in order to reveal the possible molecular mechanism. Methods: Eighty-nine male SD rats were randomly distributed into three groups: twenty-four in normal control group; thirty-three in experimental liver fibrosis model induced by CCl4 as disease control group; thirty-two in glycyrrhizin treated group. Glycyrrhizin treated group received intraperitoneal injections of glycyrrhizin twice per week. The difference of Smad7 among the three groups in different stages (1,2,4,8 weeks after injection of CCl4 ) were assessed by immunohistochemistry. Results: We identified that glycyrrhizin could improve the pathological changes of rat livers at any stage, and more apparently at the late stage. We found that glycyrrhizin could improve the expression of smad7 especially in later stage of liver fibrosis. Conclusion: Glycyrrhizin could improve the pathological changes of CCl4 induced rat liver fibrosis. The anti-fibrosis mechanism of glvcvrrhizin may be through increasing the exnression cf Smad7
出处
《中国临床医学》
北大核心
2006年第1期67-69,共3页
Chinese Journal of Clinical Medicine
基金
国家自然科学基金资助上海市科委科研基金资助