Related Experiment Video
Updated: Jun 14, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Nicotine promotes cardiomyocyte apoptosis via oxidative stress and altered apoptosis-related gene expression
Xiang Zhou1, Yanhui Sheng, Rong Yang
1Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, PR China. zx.psh@163.com
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.
Related Concept Videos
Drugs Acting on Autonomic Ganglia: Stimulants
Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating sympathetic or...
Cellular Injury V: Apoptosis and Autophagy
The Extrinsic Apoptotic Pathway
The Intrinsic Apoptotic Pathway
Cellular Injury IV: Necrosis
Apoptosis
