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Oxidative Medicine and Cellular Longevity
Volume 2018, Article ID 3685391, 11 pages
Research Article

Gastrodin Protects Cardiomyocytes from Anoxia/Reoxygenation Injury by 14-3-3η

1Jiangxi Provincial Key Laboratory of Basic Pharmacology, School of Pharmaceutical Science, Nanchang University, Nanchang 330006, China
2Key Laboratory of Women’s Reproductive Health of Jiangxi, Jiangxi Maternal and Child Health Hospital, Nanchang 330006, China
3Second Abdominal Surgery Department, Jiangxi Province Tumor Hospital, Nanchang 330029, China

Correspondence should be addressed to Dan Liu; moc.361@xj1021naduil and Bo Yi; moc.361@805097obiy

Received 7 February 2018; Revised 6 May 2018; Accepted 7 June 2018; Published 25 July 2018

Academic Editor: Jerzy Kruk

Copyright © 2018 Meifang Zhu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Gastrodin (GAS) is the major component isolated from the rhizome of the Chinese traditional medicinal herb “Tianma.” Many clinical studies have found that GAS protects cardiomyocytes in cardiovascular diseases, although the effects and underlying mechanisms on cardiovascular anoxia/reoxygenation (A/R) injury remain unknown. This study is aimed at exploring the effect of gastrodin on cardiomyocytes in A/R injury. Our results suggested that the protective effect of GAS on cardiomyocytes is associated with upregulated 14-3-3η levels. Pretreatment with GAS could increase the cell viability and decrease the activities of creatine phosphokinase (CPK) and lactate dehydrogenase (LDH). GAS could also reduce reactive oxygen species (ROS) production, inhibit mitochondrial permeability transition pore (mPTP) opening, alter the maintenance of the mitochondrial membrane potential (∆Ψm), decrease the activation of caspase-3, and finally restrain cell apoptosis. Downregulating 14-3-3η levels by transfection with siRNA14-3-3η clearly attenuated the protective effect of GAS on cardiomyocytes in A/R injury.