Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1
Joint Authors
Wang, Rui-ying
Zhou, Jia-hui
Xie, Xue-heng
Sun, Gui-bo
Sun, Xiao-bo
Wang, Min
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-12, 12 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-08-31
Country of Publication
Egypt
No. of Pages
12
Main Subjects
Abstract EN
Calenduloside E (CE) is a natural triterpenoid saponin isolated from Aralia elata (Miq.) Seem., a well-known traditional Chinese medicine.
Our previous studies have shown that CE exerts cardiovascular protective effects both in vivo and in vitro.
However, its role in myocardial ischemia/reperfusion injury (MIRI) and the mechanism involved are currently unknown.
Mitochondrial dynamics play a key role in MIRI.
This study investigated the effects of CE on mitochondrial dynamics and the signaling pathways involved in myocardial ischemia/reperfusion (MI/R).
The MI/R rat model and the hypoxia/reoxygenation (H/R) cardiomyocyte model were established in this study.
CE exerted significant cardioprotective effects in vivo and in vitro by improving cardiac function, decreasing myocardial infarct size, increasing cardiomyocyte viability, and inhibiting cardiomyocyte apoptosis associated with MI/R.
Mechanistically, CE restored mitochondrial homeostasis against MI/R injury through improved mitochondrial ultrastructure, enhanced ATP content and mitochondrial membrane potential, and reduced mitochondrial permeability transition pore (MPTP) opening, while promoting mitochondrial fusion and preventing mitochondrial fission.
However, genetic silencing of OPA1 by siRNA abolished the beneficial effects of CE on cardiomyocyte survival and mitochondrial dynamics.
Moreover, we demonstrated that CE activated AMP-activated protein kinase (AMPK) and treatment with the AMPK inhibitor, compound C, abolished the protective effects of CE on OPA1 expression and mitochondrial function.
Overall, this study demonstrates that CE is effective in mitigating MIRI by modulating AMPK activation-mediated OPA1-related mitochondrial fusion.
American Psychological Association (APA)
Wang, Min& Wang, Rui-ying& Zhou, Jia-hui& Xie, Xue-heng& Sun, Gui-bo& Sun, Xiao-bo. 2020. Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1203938
Modern Language Association (MLA)
Wang, Min…[et al.]. Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-12.
https://search.emarefa.net/detail/BIM-1203938
American Medical Association (AMA)
Wang, Min& Wang, Rui-ying& Zhou, Jia-hui& Xie, Xue-heng& Sun, Gui-bo& Sun, Xiao-bo. Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-12.
https://search.emarefa.net/detail/BIM-1203938
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1203938