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作 者:陶华[1,2] 孙新臣[3] 鲁世慧[1] 成红艳[3] 郭林[3] 袁喜[3]
机构地区:[1]东南大学医学院,江苏南京210009 [2]南京医科大学附属江苏省肿瘤医院放疗科,江苏南京210009 [3]东南大学附属中大医院放疗科,江苏南京210009
出 处:《南京医科大学学报(自然科学版)》2012年第5期669-672,共4页Journal of Nanjing Medical University(Natural Sciences)
基 金:国家自然科学基金(30970792)
摘 要:目的:研究洛铂联合放疗对非小细胞肺癌细胞的杀伤作用以及对细胞周期和凋亡的影响。方法:MTT法观察肺癌A549细胞增殖抑制,流式细胞仪检测细胞凋亡及细胞周期分布,蛋白免疫印迹检测Bcl-2和Bax蛋白表达。结果:洛铂对肺癌A549细胞有增殖抑制作用,且细胞毒性呈剂量依赖性;洛铂联合放疗组观察到有更高的细胞凋亡率和G2/M期阻滞;蛋白免疫印迹结果显示洛铂联合放疗组Bcl-2表达水平下降,促进凋亡诱导蛋白Bax表达水平升高。结论:洛铂有放疗增敏作用,作用机制可能与抑制Bcl-2表达、促进Bax表达、激活Bcl-2(Bax)-Caspase信号通路有关。Objective:To study the effect of labaplatin combined with irradiation on non-small cell lung cancer cell line A549 and explore its radiosensitizing mechanism.Methods: MTT was used to examine the effect of labaplatin and / or irradiation on lung cancer cell line A549 proliferation.Flow cytometry was applied to detect the cell cycle distribution and cell apoptosis.Western blotting was used to observe the expression of Bcl-2 and Bax.Results: Lung cancer cell line A549 could be inhibited by labaplatin in a concentration dependent manner.G2 /M phase peak and apoptosis rate was the highest in cells treated with labaplatin combined with irradiation.Western blotting illustrated the decrease of Bcl-2 and the increase of Bax.Conclusion: Labaplatin could radiosensitize A549 cells and the possible mechanism might be related with inhibiting Bcl-2,inducing Bax expression and activating the Bcl-2(Bax)-caspase signaling way.
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