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

Abstract 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 pres...

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Autores principales: Yucong Xue, Muqing Zhang, Bin Zheng, Yuanyuan Zhang, Xi Chu, Yu Liu, Ziliang Li, Xue Han, Li Chu
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Publicado: Wiley 2021
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spelling oai:doaj.org-article:8a06262274f448cd916aded92c4469382021-11-16T13:45:54Z[8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels2052-170710.1002/prp2.852https://doaj.org/article/8a06262274f448cd916aded92c4469382021-10-01T00:00:00Zhttps://doi.org/10.1002/prp2.852https://doaj.org/toc/2052-1707Abstract 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.Yucong XueMuqing ZhangBin ZhengYuanyuan ZhangXi ChuYu LiuZiliang LiXue HanLi ChuWileyarticle[8]‐gingerolcell contractilityL‐type Ca2+ currentMAPK signaling pathwaymyocardial ischemiaoxidative stressTherapeutics. PharmacologyRM1-950ENPharmacology Research & Perspectives, Vol 9, Iss 5, Pp n/a-n/a (2021)
institution DOAJ
collection DOAJ
language EN
topic [8]‐gingerol
cell contractility
L‐type Ca2+ current
MAPK signaling pathway
myocardial ischemia
oxidative stress
Therapeutics. Pharmacology
RM1-950
spellingShingle [8]‐gingerol
cell contractility
L‐type Ca2+ current
MAPK signaling pathway
myocardial ischemia
oxidative stress
Therapeutics. Pharmacology
RM1-950
Yucong Xue
Muqing Zhang
Bin Zheng
Yuanyuan Zhang
Xi Chu
Yu Liu
Ziliang Li
Xue Han
Li Chu
[8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
description Abstract 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.
format article
author Yucong Xue
Muqing Zhang
Bin Zheng
Yuanyuan Zhang
Xi Chu
Yu Liu
Ziliang Li
Xue Han
Li Chu
author_facet Yucong Xue
Muqing Zhang
Bin Zheng
Yuanyuan Zhang
Xi Chu
Yu Liu
Ziliang Li
Xue Han
Li Chu
author_sort Yucong Xue
title [8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
title_short [8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
title_full [8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
title_fullStr [8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
title_full_unstemmed [8]‐Gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the MAPK signaling pathway and L‐type Ca2+ channels
title_sort [8]‐gingerol exerts anti‐myocardial ischemic effects in rats via modulation of the mapk signaling pathway and l‐type ca2+ channels
publisher Wiley
publishDate 2021
url https://doaj.org/article/8a06262274f448cd916aded92c446938
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