Nicotine Promotes Cardiomyocyte Apoptosis via Oxidative Stress and Altered Apoptosis-Related Gene Expression
Nicotine Promotes Cardiomyocyte Apoptosis via Oxidative Stress and Altered Apoptosis-Related Gene Expression
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DOI：
10.1159/000301278
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发表时间：
2010-01-01
期刊：
影响因子：
1.9
通讯作者：
Kong, Xiangqing
中科院分区：
文献类型：
--
作者：
Zhou, Xiang;Sheng, Yanhui;Kong, Xiangqing
目的：研究尼古丁对体外心肌细胞凋亡的影响并探讨其可能机制。方法：采用MTT法检测不同浓度尼古丁（0.1 ~ 100 μ M）对培养心肌细胞的影响。采用激光共聚焦显微镜、TUNEL法和流式细胞术检测心肌细胞凋亡。通过培养基上清液中乳酸脱氢酶、丙二醛和超氧化物歧化酶的水平来评价氧化应激。Real-time PCR检测尼古丁与对照组细胞凋亡相关基因mRNA表达变化。结果：烟碱对心肌细胞活力的抑制呈浓度依赖性。结果表明，尼古丁可促进心肌细胞凋亡，抗氧化剂谷胱甘肽可通过抑制尼古丁诱导的氧化应激来保护心肌细胞凋亡。Real-time PCR结果显示，尼古丁组Bcl-2、Pax3、Bmp4、Slug表达下调，P53、Bax、Msx1表达上调。结论：尼古丁通过诱导氧化应激和破坏凋亡相关基因表达促进心肌细胞凋亡。版权所有：S. Karger AG，巴塞尔
Objective: To investigate the effect of nicotine on cardiomyocyte apoptosis in vitro and explore the potential mechanisms involved. Methods: The MTT assay was used to detect the viability of cultured cardiomyocytes exposed to different concentrations of nicotine (0.1-100 mu M). Laser confocal microscopy, TUNEL assay and flow cytometry were utilized to detect cardiomyocyte apoptosis. Oxidative stress was evaluated by the levels of lactic dehydrogenase, malondialdehyde and superoxide dismutase in the supernatant of culture media. Real-time PCR was conducted to identify mRNA expression changes in apoptosis-related genes between the nicotine and the control group. Results: Nicotine was found to inhibit cardiomyocyte viability in a concentration-dependent manner. Our results demonstrated that nicotine can promote cardiomyocyte apoptosis and the antioxidant glutathione can protect cardiomyocytes from apoptosis via inhibition of nicotine-induced oxidative stress. Real-time PCR indicated that the expression of Bcl-2, Pax3, Bmp4 and Slug was down-regulated in the nicotine group, while the expression of P53, Bax and Msx1 was up-regulated. Conclusion: Nicotine promotes cardiomyocyte apoptosis by inducing oxidative stress and disrupting apoptosis-related gene expression. Copyright (C) 2010 S. Karger AG, Basel