摘要
目的 观察烟草烟雾中的主要有害成分尼古丁对人A549细胞增殖、迁移与侵袭能力的影响,探讨尼古丁致病的可能机制.方法 以一定浓度尼古丁刺激体外培养的人A549细胞,应用CCK-8法、Transwell法和细胞划痕实验分别检测A549细胞的增殖、侵袭及迁移能力.Western blot检测α7烟碱型乙酰胆碱受体(α7 nAChR)、血管内皮生长因子(VEGF)和基质金属蛋白酶2(MMP-2)蛋白的表达.结果 与空白对照组比较,10^-6 mol/L尼古丁处理A549细胞后,促进人A549细胞增殖(t=7.920,P〈0.05);使穿过基质胶的细胞数增多,侵袭能力增强(t=5.298,P〈0.05);使细胞迁移率增加,迁移能力增强(P〈0.05).与空白对照组比较,10^-6 M尼古丁处理A549细胞24 h后,α7 nAChR、VEGF和MMP-2蛋白表达上调,差异有统计学意义(t值分别为5.800、4.074、6.851,P值均〈0.05).结论 尼古丁通过其特异性受体α7 nAChR可增强人A549细胞的增殖、侵袭和迁移能力,其机制可能与VEGF和MMP-2蛋白表达上调有关.
Objective To study the effects of nicotine on cell proliferation,invasion and migration of A549 and explore the possible mechanisms.Methods The abilities of proliferation,migration and invasion of A549 cell were measured by CCK-8,Transwell test,and wound scratch assay respectively.The expressions ofα7 nicotinic acetylcholine receptor (nAChR),vascular endothelial growth factor (VEGF) and matrix metalloproteinase-2 (MMP-2) were observed by Western blot.Results Compared with the control group,10-6 mol/L nicotine promoted A549 proliferation,migration and invasion significantly (all P 〈0.05).Nicotine increased the protein expressions ofα7 nAChR,VEGF and MMP-2.Conclusions Nicotine can increase proliferation,migration and invasion of human lung adenocarcinoma A549 cell throughα7 nAChR,which may be associated with the upregulation of VEGF and MMP-2 protein expressions.
出处
《国际呼吸杂志》
2017年第4期241-245,共5页
International Journal of Respiration
基金
国家自然科学基金(81470233、81570035)
广东省自然科学基金-重点(2014A030311040)
广州医科大学自然科学青年项目(2015A10)
关键词
尼古丁
细胞增殖
细胞侵袭
细胞迁移
Nicotine
Cell proliferation
Cell migration
Cell invasion