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Gastrodin protects H9c2 cardiomyocytes against oxidative injury by ameliorating imbalanced mitochondrial dynamics and mitochondrial dysfunction

Authors: Qiao-qiao Cheng1, Yu-wei Wan1, Wei-min Yang2, Meng-hua Tian3, Yu-chuan Wang3, Hai-yan He3, Wei-dong Zhang1, Xuan Liu1
1 Institute of Interdisciplinary Integrative Biomedical Research, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
2 School of Pharmaceutical Science and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming 650500, China
3 Zhaotong Institute of Tianma, Zhaotong 657000, China

Correspondence to: Wei-dong Zhang: wdzhangy@hotmail.com, Xuan Liu: xuanliu@shutcm.edu.cn,
DOI: 10.1038/s41401-020-0382-x
Received: 1 January 1970
Accepted: 14 February 2020
Advance online: 12 March 2020

Abstract

Gastrodin (GAS) is the main bioactive component of Tianma, a traditional Chinese medicine widely used to treat neurological disorders as well as cardio- and cerebrovascular diseases. In the present study, the protective effects of GAS on H9c2 cells against ischemia–reperfusion (IR)-like injury were found to be related to decreasing of oxidative stress. Furthermore, GAS could protect H9c2 cells against oxidative injury induced by H2+O2+. Pretreatment of GAS at 20, 50, and 100 μM for 4 h significantly ameliorated the decrease in cell viability and increase in apoptosis of H9c2 cells treated with 400 μM H2+O2+ for 3 h. Furthermore, we showed that H2+O2+ treatment induced fragmentation of mitochondria and significant reduction in networks, footprint, and tubular length of mitochondria; H2+O2+ treatment strongly inhibited mitochondrial respiration; H2+O2+ treatment induced a decrease in the expression of mitochondrial fusion factors Mfn2 and Opa1, and increase in the expression of mitochondrial fission factor Fis1. All these alterations in H2+O2+-treated H9c2 cells could be ameliorated by GAS pretreatment. Moreover, we revealed that GAS pretreatment enhanced the nuclear translocation of Nrf2 under H2+O2+ treatment. Knockdown of Nrf2 expression abolished the protective effects of GAS on H2+O2+-treated H9c2 cells. Our results suggest that GAS may protect H9c2 cardiomycytes against oxidative injury via increasing the nuclear translocation of Nrf2, regulating mitochondrial dynamics, and maintaining the structure and functions of mitochondria.
Keywords: gastrodin; Tianma; H9c2 cardiomycytes; oxidative injury; Nrf2; mitochondrial dynamics; mitochondrial respiration

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