Involvement of GPR30 in protection effect of Dexmedetomidine against myocardial ischemia/reperfusion injury in rat via AKT pathway

  • Zheming Shao Department of Anesthesiology, Zhejiang Sian Internatinal Hospital, Jiaxing City, Zhejiang Province, 314000, China
  • Qihong Shen Department of Anesthesiology-Jiaxing Key Discipline of Medicine-Anesthesiology (2019-zc-06), The Affiliated Hospital of Jiaxing University, The First Hospital of Jiaxing, Jiaxing City, Zhejiang Province, 314001, China
  • Min Kong Department of Anesthesiology-Jiaxing Key Discipline of Medicine-Anesthesiology (2019-zc-06), The Affiliated Hospital of Jiaxing University, The First Hospital of Jiaxing, Jiaxing City, Zhejiang Province, 314001, China
  • Huadong Ni Department of Anesthesiology-Jiaxing Key Discipline of Medicine-Anesthesiology (2019-zc-06), The Affiliated Hospital of Jiaxing University, The First Hospital of Jiaxing, Jiaxing City, Zhejiang Province, 314001, China
  • Xiaomin Hou Department of Anesthesiology-Jiaxing Key Discipline of Medicine-Anesthesiology (2019-zc-06), The Affiliated Hospital of Jiaxing University, The First Hospital of Jiaxing, Jiaxing City, Zhejiang Province, 314001, China
DOI: https://doi.org/10.18388/abp.2020_5473

Abstract

Acute myocardial infarction (AMI) is a heart disease that seriously threatens human health. Dexmedetomidine (DEX) has a certain protective effect on cardiac injury. This study investigated the cardioprotective effect of DEX and its potential molecular mechanism in vivo and in vitro. The results showed that DEX could significantly increase the viability of hypoxia/reoxygenation (H/R) treated cardiomyocytes and reduce oxidative damage and apoptosis. Further molecular mechanism analysis showed that the above cardiac protective effects may be related to Akt signaling pathway. In addition, the expression of G-Protein Receptor 30 (GPR30) was promoted after H/R treatment. However, knockdown of GPR30 by shRNA significantly counteracted the cardioprotective effect of DEX. Meanwhile, we constructed a rat model of AMI to investigate the role of GPR30 in vivo. The results showed that DEX significantly reduced the infarct size, and GPR30 agonist G1 enhanced the protective effect of DEX on heart. On the contrary, protein kinase B (AKT) inhibitor LY294002 counteracted the protective effect of DEX on heart, suggesting that GPR30 enhanced the protective effect of DEX on ischemia-reperfusion induced heart injury by regulating AKT related pathways. In conclusion, our study provides a potential target for the clinical treatment of AMI.

Published
2021-02-25
Issue
Vol. 68 No. 1 (2021)
Section
Articles

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