Xiang Zhou1, Yanhui Sheng, Rong Yang, Xiangqing Kong. 1. Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, PR China. zx.psh@163.com
Abstract
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 microM). 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.
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 microM). 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.
Authors: Indrani Sinha-Hikim; Theodore C Friedman; Mark Falz; Victor Chalfant; Mohammad Kamrul Hasan; Jorge Espinoza-Derout; Desean L Lee; Carl Sims; Peter Tran; Sushil K Mahata; Amiya P Sinha-Hikim Journal: Cell Tissue Res Date: 2016-12-05 Impact factor: 5.249