低Se低VE诱导肝细胞凋亡及相关基因所起的作用

目的 研究低硒（Ｓｅ）低维生素Ｅ（ＶＥ）能否诱导大鼠肝细胞凋亡及相关基因ｐ５３、ｂｃｌ－２和ｃ－ｍｙｃ所起的作用。方法 以天然的和人工半合成的低Ｓｅ低ＶＥ饲料喂养大鼠１７周，采用末端脱氧核苷酸转移酶介导的缺口末端标记（ＴＵＮＥＬ）检测肝细胞凋亡，采用免疫组化法检测肝细胞ｐ５３、ｂｃｌ－２和ｃ－ｍｙｃ蛋白。结果 与补Ｓｅ和ＶＥ组大鼠相比，低Ｓｅ低ＶＥ组大鼠肝细胞凋亡显著增加；ｐ５３和ｃ－ｍｙｃ蛋白增

Hepatocyte apoptosis induced by selenium and vitamin E deficiency and the role of bcl-2 and c-myc in the apoptotic process

Objective To study whether dietary deficiency of selenium (Se) and vitamine E(VE) can induce hepatocyte apoptosis and what is the role of p53,bcl-2 and c-myc in the apoptotic process.Methods The experiment was performed on rats kept on natural or semisynthetic diet deficient in Se and VE for 17 weeks.The hepatocyte apoptosis was detected by using TUNEL in rats.The p53,bcl-2 and c-myc proteins were detected by immunohistochemistry in hepatocytes.Results As compared with Se and VE supplemented group,hepatocyte apoptosis was obviously increased in rats kept on Se and VE deficient diet,accompanied with an increased expression of p53 and c-myc protein but a lower expression of bcl-2 protein in hepatocytes.Conclusions The dietary deficiency of Se and VE can induce hepatocyte apoptosis in rats;p53,bcl-2 and c-myc may be involved in the regulation of the apoptotic process.