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Muscone suppresses myocardial ischemia damage by regulating PI3K/Akt signaling pathway.

Authors :
Zhu LL
Cao GY
Jia LY
Zheng G
Zhang L
Sheng P
Meng ZQ
He X
Zhang CF
Wang CZ
Yuan CS
Source :
Biochimica et biophysica acta. Molecular basis of disease [Biochim Biophys Acta Mol Basis Dis] 2022 Dec 01; Vol. 1868 (12), pp. 166539. Date of Electronic Publication: 2022 Sep 11.
Publication Year :
2022

Abstract

Muscone is the main active compound of Moschus. In this paper, the cardioprotective effect of Muscone on acute myocardial ischemia (AMI) rats and its potential mechanisms were investigated. AMI rat models were established to evaluate the protective effect and antioxidative function of Muscone on the hearts. Moreover, Western blot analysis was conducted to quantify the phosphorylated PI3K and AKT levels in PI3K/Akt pathway for further investigating the mechanism of Muscone. Results showed that Muscone could markedly lessen the infarct size and myocardial injury, improve cardiac function, inhibit cardiomyocyte apoptosis and down-regulate serum reactive oxygen species level as indicated by the decreased MDA, BNP and c-TnI activities and the increased SOD, GSH-px, CAT activities and the expression of Bax protein. In addition, it was revealed that Muscone notably promoted the phosphorylation of PI3K and AKT. These findings denote that Muscone exerts a protective effect in heart via inhibition of oxidative stress and apoptosis, offering new insights into the treatment of CHD and the clinical application of Muscone.<br />Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1879-260X
Volume :
1868
Issue :
12
Database :
MEDLINE
Journal :
Biochimica et biophysica acta. Molecular basis of disease
Publication Type :
Academic Journal
Accession number :
36100155
Full Text :
https://doi.org/10.1016/j.bbadis.2022.166539