探讨MG132对人肺腺癌A549细胞凋亡影响及其机制.docVIP

探讨MG132对人肺腺癌A549细胞凋亡影响及其机制 　　[摘要] 目的：研究不同浓度蛋白酶体抑制剂MG132对人肺腺癌A549细胞凋亡的作用，并且观察对细胞中Bcl-2和Bad两种凋亡相关蛋白表达的影响。方法：体外培养A549细胞分别暴露于0、5、10、20、40 μmol/L的MG132，24 h后MTT法测定细胞存活率，流式细胞术（FCW）检测细胞的凋亡率，Western Blot方法测定A549细胞中Bcl-2和Bad两种蛋白的表达情况。结果：MTT法和流式细胞术检测结果显示，A549细胞的存活率和凋亡率与MG132呈浓度依赖性关系，MG132浓度越高细胞存活率越低，并且凋亡率越高。Western Blot方法测定结果显示A549细胞中Bcl-2的表达随着MG132浓度增高而逐渐减少，而Bad的表达无明显变化。结论：MG132可以诱导人肺腺癌A549细胞的凋亡，实现该作用的可能机制部分是通过降低Bcl-2蛋白的表达，而Bad在这一过程中似乎没有表现出明显的作用。 　　[关键词] 肺腺癌；蛋白酶体抑制剂；A549细胞；Bcl-2；Bad 　　[中图分类号] R734.2；R730.54 [文献标识码] A [文章编号] 1673-7210（2011）12（a）-032-03 　　 　　The effect and mechanism on the apoptosis of adenocarcinoma of lung A549 cell treated with MG132 　　ZHU Yi, GONG Li, NIU Hongyan 　　Department of Chest Aurgery, the Second Peoples Hospital of Huaian City Affiliated of Xuzhou Medical College, Jiangsu Province, Huaian 223002, China 　　[Abstract] Objective: To study the apoptosis of adenocarcinoma of lung A549 cell treated with different concentrations of proteasomes inhibitor MG132, and to observe the expression of Bcl-2 and Bad in A549 cells. Methods: In vitro, A549 cells were exposed to 0, 5, 10, 20, 40 μmol/L of MG132. 24 hours later, the survival rate of A549 cells was detected with MTT chromatometry, flow cytometry detected the apoptosis rate of A549 cells, and the expression of Bcl-2 and Bad in A549 cells was measured with Western Blot. Results: MG132 caused the apoptosis of A549 cells in a concentration-dependent manner, the survival rate of cells was gradually decreased while the apoptosis rate of cells was increased after 24 hours exposure to MG132. Meanwhile, the expression of Bcl-2 was decreased, and the Bad expression was unchanged in A549 cells. Conclusion: MG132 could induce A549 cells apoptosis partly through depressing the expression of Bcl-2, but not promoting Bad expression. 　　[Key words] Adenocarcinoma of lung; Proteasomes inhibitor; A549 cell; Bcl-2; Bad 　　近几十年来，肺癌的发病率和死亡率不断升高。在1998~2002年，肺癌的发病率和死亡率在我国大多数地区居恶性肿瘤的首位[1]；而在2002年肺癌的新病例和死亡人数在全世界也居恶性肿瘤首