探讨MG132对人肺腺癌A549细胞凋亡的影响及其机制

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、40Ixmol／L的MGl32，24h后MTF法测定细胞存活率，流式细胞术（FCW）检测细胞的凋亡率，WesternBlot方法测定A549细胞中Bcl-2和Bad两种蛋白的表达情况。结果：MTY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MGl32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。WesternBlot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。

The effect and mechanism on the apoptosis of adenocarcinoma of lung A549 cell treated with MG132

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 ceils. 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 MTY 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-de- pendent manner, the survival rate of cells was gradually decreased while the apoptosis rate of ceils 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.