[8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels

• Published in: Pharmacology research & perspectives Vol. 9; no. 5; pp. e00852 - n/a
• Main Authors: Xue, Yucong, Zhang, Muqing, Zheng, Bin, Zhang, Yuanyuan, Chu, Xi, Liu, Yu, Li, Ziliang, Han, Xue, Chu, Li
• Format: Journal Article
• Language: English
• Published: Bognor Regis John Wiley & Sons, Inc 01.10.2021; John Wiley and Sons Inc; Wiley
• Subjects: Apoptosis; Bioengineering; Cardiomyocytes; Cardiovascular disease; cell contractility; Chemicals; Coronary vessels; Drug dosages; Electrocardiography; gingerol; Heart; Homeostasis; Ischemia; Kinases; Laboratory animals; L‐type Ca2+ current; MAPK signaling pathway; myocardial ischemia; Original; Oxidative stress; Pharmacology; Proteins; Signal transduction
• ISSN: 2052-1707; 2052-1707
• DOI: 10.1002/prp2.852

Myocardial ischemia (MI) remains the leading cause of mortality worldwide. Therefore, it is urgent to seek the treatment to protect the heart. [8]‐Gingerol (8‐Gin), one of the most active ingredients in ginger, has antioxidant, cardiotonic, and cardiovascular protective properties. The present study elucidated the cardioprotection effects and underlying mechanisms of 8‐Gin in isoproterenol (ISO)‐induced MI. ISO (85 mg/kg/d) was subcutaneously injected for 2 consecutive days to induce acute MI model in rats. Electrocardiography, oxidative stress levels, calcium concentrations, and apoptosis degree were observed. The effects of 8‐Gin on L‐type Ca2+ current (ICa‐L), contraction, and Ca2+ transients were monitored in rat myocytes via patch‐clamp and IonOptix detection systems. 8‐Gin decreased J‐point elevation and heart rate and improved pathological heart damage. Moreover, 8‐Gin reduced the levels of CK, LDH, and MDA, ROS production, and calcium concentrations in myocardial tissue, while increased the activities of SOD, CAT, and GSH. In addition, 8‐Gin down‐regulated Caspase‐3 and Bax expressions, while up‐regulated Bcl‐2 expression. 8‐Gin produced a marked decrease in the expression of p38, JNK, and ERK1/2 proteins. 8‐Gin inhibited ICa‐L, cell contraction, and Ca2+ transients in isolated rat myocytes. The results indicate that 8‐Gin could exert anti‐myocardial ischemic effects, which may be associated with oxidative stress reduction, cardiomyocytes apoptosis inhibition through MAPK signaling pathway, and Ca2+ homeostasis regulation via ICa‐L modulation. 8‐Gin has a cardioprotective effect against ISO‐induced myocardial ischemic. The underlying mechanisms were related to reducing oxidative stress, preventing cardiomyocyte apoptosis via inhibiting the MAPK signaling pathway, and suppressing Ca2+ overload through inhibiting the LTCCs.