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目的:探讨组蛋白去乙酰化酶抑制剂曲古霉素A(trichostatin A,TSA)增强人非小细胞肺癌(NSCLC)A549对γ-射线敏感性作用及机制。方法:以TSA(0.5μM)预处理细胞18h,再以5Gyγ-射线照射细胞,24h后采用MTT法检测细胞存活率,AnnexinV-PI染色检测细胞凋亡,Westemblot法检测胞浆中和线粒体促凋亡蛋白Bax的表达,流式细胞仪检测细胞线粒体膜电位变化。结果:5Gyγ-射线照射可轻度降低细胞存活率,仅有少量细胞发生凋亡,以TSA预处理再以γ-射线处理细胞,细胞存活率显著下降,凋亡细胞明显增多,伴有线粒体膜电位下降,以及Bax蛋白的激活,表现在线粒体Bax表达较单纯照射组显著增高。结论:TSA通过促进Bax蛋白的活化激活线粒体凋亡途径,增强增强A549细胞对y-射线的敏感性。
AIM: To investigate the effect of histone deacetylase inhibitor trichostatin A (TSA) on γ-ray sensitivity of human non-small cell lung cancer (NSCLC) A549 and its mechanism. Methods: The cells were pretreated with TSA (0.5μM) for 18h, then irradiated with 5Gy γ-rays. The cell viability was detected by MTT assay after 24 hours. The apoptosis was detected by Annexin V-PI staining and the mitochondria were detected by Westemblot assay. The expression of Bax protein was detected by flow cytometry and the mitochondrial membrane potential was measured by flow cytometry. Results: 5Gyγ-ray irradiation could slightly reduce the cell survival rate, only a small number of cells apoptosis, TSA pretreatment and then γ-ray treatment cells, cell viability decreased significantly, apoptotic cells increased significantly, accompanied by mitochondrial membrane Potential decline, as well as Bax protein activation, the expression of mitochondrial Bax expression was significantly higher than the simple irradiation group. Conclusion: TSA activates the mitochondrial apoptotic pathway through the activation of Bax protein and enhances the sensitivity of A549 cells to y-ray.