Nicotine promotes cardiomyocyte apoptosis via oxidative stress and altered apoptosis-related gene expression.

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.