摘要
目的 研究高铁负荷对化学性肝损伤大鼠Bcl 2 /Bax基因表达的影响。方法 复制大鼠高铁负荷模型 ,以四氯化碳 (CCl4)攻击复制肝损伤模型。观察各实验组和对照组的血清铁 (SI)、肝组织铁 (HIC)及丙二醛 (MDA)含量变化 ,流式细胞仪检测肝细胞DNA含量、Bcl 2和Bax表达量 ,计算凋亡指数 (ApoptoticIndex ,AI)和增殖指数 (ProliferationIndex ,PI)。结果 高铁组大鼠SI,HIC及MDA含量增加 ,AI升高 ,PI无明显变化。CCl4+高铁组与高铁组相比 ,MDA ,AI及Bax均有显著增加。结论 铁可以诱导肝细胞凋亡 ,其机制可能为 :上调促凋亡基因Bax水平 ,催化脂质过氧化反应 ,促进氧自由基的产生 ,从而引起肝细胞凋亡 ,并且 ,铁与CCl4在促进肝细胞凋亡上有协同作用。
Objective To investigate the hepatocytes apoptosis mechanism induced by iron overload. Methods Rats 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 malondealdehyde (MDA) levels were evaluated. Besides hepatocytes apoptotic index (AI), proliferation index (PI) and Bcl 2/Bax expression were detected with the help of flow cytometry. Results Comparison with control group, not only SI, HIC and MDA increased, but AI and Bax expression were raised, while PI had no significant change in ID injection group. In addition, MDA, AI and Bax were elevated more significantly in CCl 4 and ID injection group than in single ID injection group. Conclusion It was found that iron may induce the hepatocytes apoptosis by promoting Bax expression and catalyzing lipid peroxidation reaction to produce free radial. Moreover, iron and CCl 4 have coordinated function to apoptosis.
出处
《临床军医杂志》
CAS
2001年第3期4-6,共3页
Clinical Journal of Medical Officers
