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目的 探讨阿霉素对肝细胞的损伤机制及亚硒酸钠对肝细胞的保护作用。方法 通过复制大鼠阿霉素性心肌损伤的动物模型，以亚硒酸钠作为保护因素，应用原位末端标记法（ Ｔ Ｕ Ｎ Ｅ Ｌ）和免疫组化技术检测大鼠肝细胞凋亡和肝细胞转化生长因子 β１ 表达，并观察了大鼠血清中脂质过氧化含量。结果 阿霉素组大鼠肝组织可见细胞凋亡和肝细胞中转化生长因子 β１ 的异常表达；阿霉素组大鼠血清中脂质过氧化物明显升高；亚硒酸钠对阿霉素的损伤有明显的保护作用。结论 阿霉素诱导肝细胞凋亡可能是其肝脏损伤机制之一，并且细胞凋亡与转化生长因子 β１的高表达和血清中脂质过氧化水平升高有密切关系。
Objective To investigate the mechanism of daunomycin on hepatocytes and the protective effect of sodium selenite on hepatocytes. Methods Rat model of doxorubicin-induced myocardial injury was established. Sodium selenite was used as the protective factor. TUNEL and immunohistochemistry were used to detect the apoptosis of hepatocytes The expression of transforming growth factor β1 in hepatocytes was observed, and the level of lipid peroxidation in rat serum was also observed. Results The apoptosis of hepatocytes and the expression of TGF-β1 in hepatocytes were observed in adriamycin-treated rats. The levels of lipid peroxides in adriamycin-treated rats were significantly increased. The effects of sodium selenite on adriamycin The damage has a significant protective effect. Conclusion Adriamycin-induced hepatocyte apoptosis may be one of the mechanisms of hepatic injury. And apoptosis is closely related to the high expression of TGF-β1 and the increase of serum lipid peroxidation level.