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NADH在辐射诱导的L02肝细胞凋亡损伤中的防护作用

PRELIMINARY STUDY OF ANTI-APOPTOSIS EFFECTS OF NADH ON L02 LIVER CELL INJURY INDUCED BY IONIZING RADIATION
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摘要 为研究细胞辅酶NADH在细胞辐射凋亡损伤中的防护作用 ,将L0 2肝细胞经 5 0Gy照射后加入不同浓度 (0~ 6 0 0 μg/ml)的NADH ,培养 6、12、2 4h ,观察细胞凋亡率并检测 3组Fas,Bax ,Bcl 2蛋白表达 ,透射电镜观察细胞凋亡形态。结果表明 ,辐射可以诱导细胞凋亡损伤 ,NADH抑制细胞辐射诱导的凋亡呈剂量依赖性 ,并可以上调Bcl 2蛋白和下调Fas、Bax蛋白表达。提示NADH对L0 2肝细胞有明显的抗辐射凋亡损伤作用 ,其作用机制可能与Fas、Bcl To study the anti apoptosis effect of NADH on normal cell line, L02 liver cells were cultured in RPMI 1640, then it was exposed to X radiation at a dose of 5 0 Gy(500cGy/min). Culture was continued in the presence or absence of different concentrations of NADH for 6, 12, 24 hours Three groups were divided as following: In Exp Ⅰ the culture was not radiated. Cells in Exp Ⅱ?Ⅲ were respectively cultured in the presence of RPMI 1640 and NADH (400μg/ml) for 24 hours after being irradiated Proteins of Fas, Bcl 2 and Bax expressed in the L02 cells were determined with flow cytometry analysis There were a variety of morphological changes in L02 cells after X ray irradiation NADH could obviously inhibit the apoptosis of L02 liver cell line in a dose dependant manner, significantly upregulate the expression of Bcl 2 protein, downregulate the expression of Fas and Bax proteins of L02 cells after irradiation( P <0 05) NADH could prevent L02 liver cells from apoptosis induced by ionizing radiation, and it might be associated with Fas,Bcl 2 and Bax gene regulation
出处 《解放军医学杂志》 CAS CSCD 北大核心 2002年第3期203-205,共3页 Medical Journal of Chinese People's Liberation Army
基金 全军医学科研"十五"计划基金资助课题 (编号 0 1MA1 38)
关键词 还原型类酰胺腺嘌呤二核苷酸 辐射防护 脱噬作用 肝细胞株 L02细胞 NADH nicotinamide adenine dinucleotide reduced radiation protection apoptosis L02 liver cell
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