Agonists of G protein-coupled receptor 120 ameliorates high glucose-induced corpus cavernous endothelial cells dysfunction via β-Arrestin2 pathway
Objective To investigate the effect of activating G protein-coupled receptor(GPR)120 on the repair of high glucose-induced endothelial injury in the human corpus cavernous,with a view to providing theoretical basis for finding new drug development targets for diabetes mellitus induced erectile dysfunction(DMED)patients.Methods The discarded cavernous tissue from patients undergoing penile prosthesis implantation surgery were collected for primary culture of corpus cavernous endothelial cells.Endothelial cell injury was induced with high concentrations of glucose,and then treated with GPR120 agonists.The cellular nitric oxide(NO)emissions,cell migration,angiogenesis functions were observed and compared in different treatment.Results Human corpus cavernous endothelial cells were successfully extracted for primary culture and identified.GPR120 was found to be stably expressed in human corpus cavernous endothelial cells with colocalization with endothelial nitric oxide synthase(eNOS).Compared with the high glucose injury group,the GPR120 agonists treated group showed significant increases in NO emissions,scratch healing rate,and angiogenesis rates(P＜0.05).After silencing β-arrestin2,GPR120 agonists lost their original therapeutic effects.Conclusions High glucose culture induces corpus cavernous endothelial cells dysfunction,and GPR120 agonists can treat corpus cavernous endothelial cells dysfunction.After silencing of β-arrestin2,GPR120 agonists fail to improve endothelial function.
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维普
