Glycyrrhizic acid exerts protective effects against hypoxia/reoxygenation‑induced human coronary artery endothelial cell damage by regulating mitochondria

Tang,Quan; Cao,Yuping; Xiong,Wei; Ke,Xixian; Zhang,Jian; Xia,Yu; Liu,Daxing

doi:10.3892/etm.2020.8668

Glycyrrhizic acid exerts protective effects against hypoxia/reoxygenation‑induced human coronary artery endothelial cell damage by regulating mitochondria

Authors:
- Quan Tang
- Yuping Cao
- Wei Xiong
- Xixian Ke
- Jian Zhang
- Yu Xia
- Daxing Liu
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Affiliations: Department of Imaging, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China, Department of Cardiac Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China
Published online on: April 15, 2020 https://doi.org/10.3892/etm.2020.8668
Pages: 335-342
Copyright: © Tang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Hypoxia/reoxygenation (H/R) is one of the main causes of coronary artery disease (CAD), which is primarily induced by damage to coronary artery endothelial cells (CAECs). Glycyrrhizic acid (GA) is a natural and abundant pentacyclic triterpenoid glycoside of the licorice root extract, and it has been reported to elicit protective effects against hypoxia, inflammation and apoptosis in ischemic myocardium; therefore, GA may serve as a promising therapeutic agent for ischemia‑associated CAD. In the present study, the protective effects of GA against H/R‑induced injury in CAECs were investigated. Treatment with GA during H/R maintained cell viability and decreased H/R‑induced cell apoptosis in human CAECs. In addition, H/R‑mediated induction of intracellular and mitochondrial reactive oxygen species (ROS) was significantly decreased by GA exposure. Similar to ROS scavengers, GA treatment not only exhibited protective effects, but also maintained the mitochondrial membrane potential after H/R and inhibited H/R‑induced mitochondrial dysfunction, including deficits in ATP synthesis, mitochondrial DNA copy number and mitochondrial transcriptional activity. Furthermore, GA decreased autophagy/mitophagy, and its protective effect against H/R was abolished by autophagy promotion. Collectively, the results suggested that GA exhibited protective effects against H/R‑induced CAEC injury by decreasing ROS accumulation and maintaining mitochondrial homeostasis. Further investigation into the precise mechanisms underlying the decrease in ROS accumulation induced by GA is required.

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