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Original Research Article | OPEN ACCESS

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Jijun Wu1, Yingli Zhou2 , Ming Guo1, Jie Yang1, Feifei Wu1, Jialin Wang1

1Department of Cardiology, Affiliated Xiaoshan Hospital, Hangzhou Normal University, Hangzhou, Zhejiang Province 310000, China; 2Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, Zhejiang Province 310000, China.

For correspondence:-  Yingli Zhou   Email: ylzhou5701@163.com   Tel:+8657187814481

Accepted: 16 July 2022        Published: 28 August 2022

Citation: Wu J, Zhou Y, Guo M, Yang J, Wu F, Wang J. Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway. Trop J Pharm Res 2022; 21(8):1601-1606 doi: 10.4314/tjpr.v21i8.4

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the protective role of tectorigenin in myocardial ischaemia/reperfusion.
Methods: Myocardial cells (H9c2) were treated with different concentrations of tectorigenin and exposed to hypoxia/reoxygenation. Cell viability and apoptosis were determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, respectively. Oxidative stress and inflammation were evaluated using enzyme-linked immunosorbent assay (ELISA), while autophagy and the underlying mechanisms of action were evaluated by Western blot.
Results: Tectorigenin enhanced the proliferative activity of H9c2 under hypoxia/reoxygenation conditions, and significantly reduced the apoptotic activity (p < 0.001) through decrease in Bax and increase in Bcl-2. Tectorigenin also significantly up-regulated SOD (superoxide dismutase) and GSH (glutathione) levels (p < 0.01), and down-regulated MDA (malondialdehyde) and MPO (myeloperoxidase) in hypoxia/reoxygenation-induced H9c2. TNF-α (tumor necrosis factor-α), IL(interleukin)-1β, and IL-6 levels were also inhibited by tectorigenin by down-regulating p-p65. Hypoxia/reoxygenation-induced increase in p62 and decrease in Beclin-1 and LC3-II/LC3-I were reversed by tectorigenin. Protein expressions of p-mTOR, p-AKT, and p-PI3K in hypoxia/reoxygenation-induced H9c2 were elevated by tectorigenin.
Conclusion: Tectorigenin exerts anti-oxidant, anti-inflammatory, and anti-autophagic effects on hypoxia/reoxygenation-induced H9c2 through the activation of PI3K/AKT/mTOR pathway, thus suggesting that it is a potential agent for the management of myocardial ischaemia/reperfusion.

Keywords: Tectorigenin, Oxidative stress, Inflammation, Autophagy, Hypoxia/reoxygenation, Myocardial cells, PI3K/AKT/mTOR

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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