摘要
目的:探讨青蒿琥酯抗肝纤维化的可能机制。方法:采用四氯化碳致小鼠肝纤维化模型,利用免疫组化和脱氧核糖核苷酸末端转移酶介导的缺口末端标记法对肝星状细胞的增生和凋亡基因进行检测。结果:青蒿琥酯高剂量组能明显降低PCNA的表达(P<0.01),确能促进凋亡基因的表达(P<0.01)。结论:青蒿琥酯对实验性肝纤维化具有明显的抑制作用,其机制可能是一方面通过抑制活化的肝星状细胞的增殖,另一方面通过调节凋亡基因的表达,进而减轻活化的肝星状细胞的增殖,恢复了凋亡和增殖的平衡态,从而起到抗肝纤维化的作用。
Objective： To find the mechamisms of artesunate＇s resistance to hepatic fibrosis. Method： The hepatic fibrosis mice model were established by carbon tetrachlorid. The apoptosis and proliferation genes of hepatic stellate cellls were detected by immunohistochemistry and the method of terminal deoxyribonucleotide transferase mediated nick and labelling. Result： The high dosage of artesunate group could significantly reduce the expression of PCNA （ P 〈 0.01 ）, and it could actually promote the expression of apoptosis genes（ P 〈 0.01 ）. Conclusion： Artesunate has a signifiantly suppressing function on the experimental fibrosis of liver. The mechamism might be inhibiting the activated proliferation of hepatic stellate eellls and regulating the expression of apoptosis genes to reduce the proliferation of hepatic stellate cellls, resulting in the rebalance of apoptosis and proliferation and finally resisting the hepatic fibrosis.
出处
《河南中医》
2009年第5期447-449,共3页
Henan Traditional Chinese Medicine
基金
广东省中医药管理局资助课题(编号:2007342)
关键词
肝纤维化
青蒿琥酯
肝脏星状细胞
凋亡
增生
小鼠
hepatic fibrosis
artesunate
hepatic stellate cellls
apoptosis
proliferation
mice
