硒对镉诱导肾细胞凋亡及其相关蛋白bcl-2、p53表达的影响
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江苏省科技厅自然科学基金资助项目(BK2001121)


Effects of selenium on cadmium-induced apoptosis and the expression of bcl-2,p53 in LLC-PK1 cells
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    目的:探讨硒对镉诱导肾小管上皮细胞(LLC-PK1)凋亡及其凋亡相关蛋白bcl-2和p53表达的影响。方法:采用四甲基偶氮唑盐(MTT)比色法检测硒对镉抑制LLC-PK1细胞生长的影响,AO/EB荧光双染法观察硒对镉诱导细胞凋亡形态的作用,并通过免疫印迹法检测凋亡相关蛋白bcl-2和p53表达水平的变化。结果:不同浓度硒对镉的细胞毒性具有一定的拮抗作用,并呈剂量效应关系; 40 μmol/L镉可诱导LLC-PK1细胞凋亡,当加入20 μmol/L硒预处理30 min再染镉12 h后,细胞凋亡的程度与单独染镉组相比有所减弱。检测凋亡相关蛋白bcl-2和p53的表达,发现镉可上调p53蛋白表达及下调bcl-2蛋白的表达,当加入硒预处理后可对镉引起的p53蛋白上调具有一定的抑制作用,但硒对镉引起的bcl-2蛋白下调作用不明显。结论:硒可拮抗镉性肾细胞凋亡,其机制可能与抑制镉引起促凋亡蛋白p53的上调有关。

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    Objective:To determine the effect of selenium on apoptosis and the expression of bcl-2,p53 induced by cadmium in LLC-PK1 cells. Methods:MTT assay was used to observe the effects of selenium on growth inhibition induced by cadmium in LLC-PK1 cells. The effect of selenium was observed in cadmium-induced apoptosis with the fluoromi croscope dyed by acridine orange/ethidium bromide(AO/EB), and the levels of p53 and bcl-2 proteins were detected by Western blot. Results:Selenium inhibited cadmium-induced LLC-PK1 cells growth in a dose-dependent manner, and the selenium pretreatment partially inhibited the cadmium-induced apoptosis. On exposure to 40 μmol/L cadmium for 12 h, the expression levels of p53 proteins were upregulated. At the same time, the level of bcl-2 protein was downregulated in LLC-PK1 cells. The selenium pretreatment inhibited the cadmiumd-induced p53 proteins upregulation, however, did not affect the bcl-2 expression levels. Conclusion:The results indicate that the protective effect of selenium may be related to the inhibition the p53 protein upregulation in cadmium-induced apoptosis.

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刘 艳,张世蘋,蔡云清.硒对镉诱导肾细胞凋亡及其相关蛋白bcl-2、p53表达的影响[J].南京医科大学学报(自然科学版),2007,(3):224-227

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  • 收稿日期:2006-08-28
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