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Protective Roles and Mechanisms of Taurine on Myocardial Hypoxia/Reoxygenation-Induced Apoptosis
Xiaohong Yang1, Jingjing Fu1,2, Huifang Wan3
1Department of Biochemistry and Molecular Biology, School of Basic Medical, Nanchang University.
Background:
This study aimed to investigate the protective roles and mechanisms of taurine on myocardial ischemia/reperfusion (I/R)-induced cell apoptosis, and thus provide evidence for the treatment of myocardial I/R injury and the development of related drugs.
Methods:
The cardiomyocytes of neonatal rats were used to prepare the hypoxia/reoxygenation (H/R) injury model; gene transfection and small interfering RNA (siRNA) target gene silencing techniques were performed, along with methyl thiazolyl tetrazolium (MTT) assay to detect cell survival, flow cytometry to detect cell apoptosis, and Western blot to measure protein expressions.
Results:
Compared with the H/R group, the apoptosis rates of cardiomyocytes in the three taurine (TAU)-protection groups were significantly decreased (p < 0.05). As the TAU concentration increased, the expression of Bcl-2 protein in H/R cardiomyocytes also gradually increased (p < 0.05), while the protein expressions of p53 up-regulated modulator of apoptosis (PUMA), C/EBP homologous protein (CHOP), Bax, glucose-regulated protein 78kD (GRP78), and caspase-3 gradually decreased (p < 0.01). TAU strongly downregulated the expression of PUMA-transfected cardiomyocytes. After targeted silencing of PUMA, the apoptosis rate was significantly decreased, while the expression of Bcl-2 protein was increased, and that of Bax protein was decreased (p < 0.05).
Conclusions:
TAU significantly inhibited myocardial H/R-induced apoptosis, and the mechanism may be related to a downregulated expression of PUMA.
Insights
Taurine (TAU) protects heart cells from injury caused by ischemia/reperfusion (I/R). It reduces apoptosis by downregulating PUMA, offering potential for treating myocardial I/R injury.
Area of Science:
- Cardiovascular Science
- Cell Biology
- Pharmacology
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a significant clinical problem.
- Cell apoptosis plays a crucial role in the pathogenesis of I/R injury.
- Taurine (TAU) is investigated for its potential cardioprotective effects.
Purpose of the Study:
- To investigate the protective effects of taurine against hypoxia/reoxygenation (H/R)-induced apoptosis in cardiomyocytes.
- To elucidate the underlying mechanisms of taurine's protective action, focusing on apoptosis-related proteins.
Main Methods:
- Neonatal rat cardiomyocytes were subjected to a hypoxia/reoxygenation (H/R) injury model.
- Cell viability was assessed using MTT assay.
- Apoptosis rates were measured by flow cytometry.
- Protein expression levels of Bcl-2, PUMA, CHOP, Bax, GRP78, and caspase-3 were analyzed by Western blot.
- Gene silencing of PUMA using siRNA was performed.
Main Results:
- Taurine significantly reduced H/R-induced cardiomyocyte apoptosis.
- Taurine treatment increased Bcl-2 expression and decreased the expression of PUMA, CHOP, Bax, GRP78, and caspase-3 in a dose-dependent manner.
- Silencing PUMA mimicked the protective effects of taurine, reducing apoptosis and altering Bcl-2 and Bax expression.
Conclusions:
- Taurine exhibits significant cardioprotective effects against H/R-induced apoptosis.
- The mechanism involves the downregulation of PUMA expression.
- Taurine holds promise as a therapeutic agent for myocardial I/R injury.
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