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为了评价在缺乏谷胱甘肽情况下硒(Se)对凋亡的影响。用睾丸细胞作为评价细胞模型。研究时,细胞被保持在各种不同处理条件下4 h,即Se(0.5μmol和1.5μmol)、BSO(20 nmol)、Se+BSO联合处理(0.5μmol Se+20 nmolBSO和1.5μmol Se+20 nmol BSO,收集被处理过的细胞,评价指标为:细胞生存能力、还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)、氧化还原率、活性氧的产生和DNA的完整性。提取JNK、p38、caspase 3和Bcl-2的mRNA进行RT-PCR分析。将对照组和处理组细胞进行比较,观察到在联合处理组伴随着GSH水平降低细胞的生存能力减弱,GSSG水平升高,活性氧(ROS)产生增加。伴随着caspase 3表达增加和Bcl-2表达减少,JNK和p38MAPK的mRNA表达增加。联合处理组细胞的DNA完整性改变。因此,本结果和早期报道观点是一致的,即细胞内活性氧(ROS)的增加可以调节由亚硒酸钠导致的细胞凋亡和硒的细胞毒性。Se处理细胞内GSH的减少也伴随凋亡增加、p38和JNK MAPK表达增加,Bcl-2表达减少,caspase-3表达增加。数据显示GSH参与睾丸细胞凋亡,GSH分子的减少在决定细胞凋亡方面起着关键的作用。
To assess the effect of selenium (Se) on apoptosis in the absence of glutathione. Testicular cells were used as evaluation cell models. At the time of the study, the cells were maintained under various treatment conditions for 4 h, ie Se (0.5 μmol and 1.5 μmol), BSO (20 nmol), Se + BSO combined treatment (0.5 μmol Se + 20 nmol BSO and 1.5 μmol Se + 20 nmol BSO, collected cells were processed, evaluation indicators: cell viability, reduced glutathione (GSH), oxidized glutathione (GSSG), redox rate, the generation of reactive oxygen species and DNA integrity The mRNA of JNK, p38, caspase 3 and Bcl-2 was extracted for RT-PCR analysis.Compared with the control group and the treated group, we found that in the combined treatment group, the viability of cells accompanied by GSH level decreased and the GSSG level Increased reactive oxygen species (ROS) production.With the increase of caspase 3 expression and the decrease of Bcl-2 expression, the mRNA expression of JNK and p38MAPK increased.The DNA integrity of cells in combination group changed.Therefore, Is consistent with the fact that an increase in intracellular reactive oxygen species (ROS) regulates apoptosis induced by sodium selenite and cytotoxicity of selenium.The reduction of GSH in Se-treated cells is accompanied by increased apoptosis, expression of p38 and JNK MAPK Increase, decrease Bcl-2 expression and increase caspase-3 expression Shows GSH involved in testicular apoptosis, reduction of GSH molecules play a critical role in determining apoptosis.