Open AccessProtective effects of 18β‐Glycyrrhetinic acid against myocardial infarction: Involvement of PI3K/Akt pathway activation and inhibiting Ca 2+ influx via L‐type Ca 2+ channels
Author(s) -
Chu Sijie,
Wang Weijie,
Zhang Ning,
Liu Tong,
Li Jing,
Chu Xi,
Zuo Saijie,
Ma Zhihong,
Ma Donglai,
Chu Li
Publication year - 2021
Publication title -
food science and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 27
ISSN - 2048-7177
DOI - 10.1002/fsn3.2639
Subject(s) - protein kinase b , pi3k/akt/mtor pathway , oxidative stress , creatine kinase , apoptosis , lactate dehydrogenase , pharmacology , chemistry , myocardial infarction , medicine , contractility , endocrinology , reactive oxygen species , biochemistry , enzyme
Abstract 18β‐Glycyrrhetinic acid (18β‐GA) is a component extracted from licorice. This study aimed to evaluate the effects of 18β‐GA on isoproterenol (ISO)‐induced acute myocardial infarction in rats and mice. Two consecutive days of subcutaneous injection of ISO (85 mg/kg/day) resulted in acute myocardial infarction. We examined the pathological changes, oxidative stress, inflammatory response, and expression of apoptosis in mouse hearts. The expressions of phosphoinositol‐3‐kinase (PI3K), protein kinase B (Akt), and the phosphorylation levels of PI3K (p‐PI3K) and Akt (p‐Akt) were determined by western blotting. The whole‐cell patch‐clamp technique was applied to observe the L‐type Ca 2+ currents, and the Ion Optix detection system was used for cell contraction and Ca 2+ transient in isolated rat cardiac ventricular myocytes. In ISO‐induced myocardial infarction, the J‐point, heart rate, creatine kinase, lactate dehydrogenase, superoxide dismutase, catalase, malondialdehyde, glutathion, and reactive oxygen species decreased in mice after 18β‐GA treatment. 18β‐GA improved ISO‐induced morphologic pathology, inhibited the inflammatory pathway response and cardiomyocyte apoptosis, and inhibited PI3K/Akt signaling. 18β‐GA could significantly inhibit I Ca‐L , myocardial contraction, and Ca 2+ transient. This study demonstrates that 18β‐GA has cardioprotective effects on acute myocardial infarction, which may be related to inhibiting oxidative stress, inflammation, apoptosis via the PI3K/Akt pathway, and reducing cell contractility and Ca 2+ concentration via L‐type Ca 2+ channels.