bcl-2/bax基因在铁诱导肝细胞凋亡中的作用

目的：研究bcl-2,bax基因在铁负荷诱导肝细胞凋亡中的作用。方法：右旋糖酐铁复制大鼠高铁负荷模型，以CCl4攻击，观察各实验组（高铁组，CCl4组，CCl4 高铁组）和空白对照组的血清铁（serum iron ,SI)，肝组织铁及丙二醛（malondialdehyde,MDA)含量变化，流式细胞仪检测肝细胞DNA含量，bcl-2,bax表达量，计算凋亡指数（apoptotic index,AI)和增殖指数（poliferation index,PI)，结果：高铁组不仅大鼠SI，肝组织铁及MDA含量增加，而且AI升,.bax水平上调，PI无明显变化，CCl4 高铁组与高铁组相比，MDA，AI,bax均有显著增加。结论：高铁负荷诱导肝细胞亡的机制可能为：上调促凋亡基因bax水平，催化脂质过氧化反应，促进氧自由基产生，铁负荷与CCl4有引起肝细胞凋亡的作用。

THE FUNCTION OF bcl-2/bax GENE IN HEPATOCYTES APOPTOSIS INDUCED BY IRON

ObjectiveTo study the action of bcl 2/bax in the hepatocytes apoptosi induced by iron overload.MethodsRats models were made with iron dextran (ID) through intraperitoneal injection or with CCl 4 through intracutaneous injection, or with both of them. Then serum iron (SI), hepatic iron concentration (HIC) and malondialdehyde (MDA) levels were observed in experimental groups (iron overload, CCl 4 and CCl 4+ iron overload groups) and blank group. The hepatocytes apoptotic index (AI), proliferation index (PI) and bcl 2/bax expression were detected with flow cytometrie methed. ResultsThe increased SI, HIC and MDA levels, higher AI and bax expression could be found in ID injection group,while no significant change in PI was seen in the group. In addition, MDA, AI and bax were elevated more significantly in CCl 4 and ID injection group than in single ID injection group.ConclusionIt was found that iron overload may induce hepatocyte apoptosis by promoting bax expression and catalyzing lipid peroxidation reaction to produce free radial. Moreover, iron overload and CCl 4 have coordinated function to hepatocyte apoptosis.