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目的:探讨白藜芦醇(resveratrol,Res)对肺腺癌A549细胞的作用及机制。方法:用不同浓度Res处理A549细胞24h后,倒置显微镜观察细胞形态学变化,DAPI细胞核染色后荧光显微镜观察细胞凋亡特征,MTT检测Res对于A549细胞生长的抑制作用,蛋白质印迹法检测Res作用A549细胞后p53、Bax、Bcl-2和Cleaved-Caspase3蛋白的表达变化。结果:Res处理A549细胞后,细胞间隙变大,细胞核裂,随着药物浓度的增加上述形态变化明显;同时DAPI染色结果提示,Res诱导A549细胞凋亡。25~200μmol/L浓度的Res可明显抑制A549细胞的增殖,25μmol/L时细胞抑制率为12.4%,50μmol/L时为21.6%,100μmol/L时为51.3%,200μmol/L时为89.7%,具有剂量依赖性。24h的IC50为98μmol/L。而且细胞内的p53、Bax和Cleaved-Caspase3蛋白的表达量升高,Pearson相关系数r值分别为0.930和0.874,P值均<0.001;Bcl-2蛋白被抑制,Bcl-2/Bax比值下降,Pearson相关系数r=0.753,P=0.01。结论:Res抑制A549细胞增殖并通过p53途径诱导A549细胞凋亡,Bax、Bcl-2和Cleaved-Caspase3参与了凋亡过程。
Objective: To investigate the effect and mechanism of resveratrol (Res) on lung adenocarcinoma A549 cells. Methods: The A549 cells were treated with different concentrations of Res for 24 h, and the morphological changes of the cells were observed by inverted microscope. The apoptotic characteristics of A549 cells were observed by fluorescence microscope after DAPI staining. The effect of Res on A549 cells was detected by MTT assay. The changes of p53, Bax, Bcl-2 and Cleaved-Caspase3 proteins after the cells were observed. Results: After A549 cells were treated with Res, the cell gap became larger and the nuclei were fissured. The morphological changes were obvious with the increase of drug concentration. Meanwhile, the results of DAPI staining indicated that Res induced A549 cell apoptosis. The proliferation of A549 cells was inhibited by 25 ~ 200μmol / L resveratrol. The cell proliferation rate was 12.4% at 25μmol / L, 21.6% at 50μmol / L, 51.3% at 100μmol / L and 89.7% at 200μmol / , In a dose-dependent manner. The IC50 for 24h is 98 μmol / L. Moreover, the expression of p53, Bax and Cleaved-Caspase3 in the cells increased, the Pearson correlation coefficient r values were 0.930 and 0.874 respectively (P <0.001), the Bcl-2 protein was inhibited and the Bcl-2 / Bax ratio decreased Pearson correlation coefficient r = 0.753, P = 0.01. CONCLUSION: Res inhibits the proliferation of A549 cells and induces the apoptosis of A549 cells through p53 pathway. Bax, Bcl-2 and Cleaved-Caspase3 are involved in the process of apoptosis.