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低Se低VE诱导肝细胞凋亡及相关基因所起的作用 被引量:2

Hepatocyte apoptosis induced by selenium and vitamin E deficiency and the role of bcl-2 and c-myc in the apoptotic process
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摘要 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 p5 3、bcl- 2和 c- m yc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 (TU NEL )检测肝细胞凋亡 ,采用免疫组化法检测肝细胞 p5 3、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 ;p5 3和 c- m yc蛋白增加 ,而 bcl- 2蛋白则仅见少量表达。结论 微量营养素 Se和 VE缺乏可诱导大鼠肝细胞凋亡 ;p5 3、bcl- 2和 c- myc可能参与这类细胞凋亡的调控。 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.
出处 《中国地方病学杂志》 CAS CSCD 2000年第4期257-259,共3页 Chinese Jouranl of Endemiology
基金 国家"八五"科技攻关专题资助!( 85 -917-0 1-0 1)
关键词 维生素E 肝细胞 细胞凋亡 诱导 Selenium Vitamin E Apoptosis
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