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

Zheming Shao | Zendy; Qi-Hong Shen | Zendy; Min Kong | Zendy; Huadong Ni | Zendy; Xiaomin Hou | Zendy

Open Access

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

Author(s) -

Zheming Shao,

Qi-Hong Shen,

Min Kong,

Huadong Ni,

Xiaomin Hou

Publication year - 2021

Publication title -

acta biochimica polonica

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.452

H-Index - 78

eISSN - 1734-154X

pISSN - 0001-527X

DOI - 10.18388/abp.2020_5473

Subject(s) - protein kinase b , cardioprotection , pharmacology , reperfusion injury , ly294002 , gper , agonist , in vivo , medicine , dexmedetomidine , pi3k/akt/mtor pathway , ischemia , myocardial infarction , apoptosis , chemistry , receptor , estrogen receptor , biology , biochemistry , microbiology and biotechnology , cancer , breast cancer , sedation

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.

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