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Objective:To investigate the protective effect of glucagon-like peptid-1(GLP-l) against cardiac microvascular endothelial cell(GTFCs) injured by high glucose.Methods:CMECs were isolated and cultured.Superoxide assay kit and dihydroethidine(DHE) staining were used to assess oxidative stress.TENEL staining and caspase 3 expression were used to assess the apoptosis of CMECs.H89 was used to inhibit eAMP/PKA pathway:fasudil was used to inhibit Rho/ROCK pathway.The protein expressions of Rho.ROCK uere examined by Western blol analysis.lesults:High glucose increased the production of ROS.the activity of NADPH.the apoptosis rate and the expression level of Rho/ROCK in CMECs.while GLP- 1 decreased high glucose-induced ROS production.the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs,the difference were statistically significant(P<0.05).Conclusions:GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis.The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner,resulting in a subsequent decrease in the expression of NADPH oxidase.
Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cells (GTFCs) injured by high glucose. Methods: CMECs were isolated and cultured. Promperoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TENEL staining and caspase 3 expression were used to assess the apoptosis of CMECs.H89 was used to inhibit eAMP / PKA pathway: fasudil was used to inhibit Rho / ROCK pathway.The protein expressions of Rho.ROCK ue examined by Western blol analysis. results: High glucose increased the production of ROS. the activity of NADPH. the apoptosis rate and the expression level of Rho / ROCK in CMECs. while GLP- 1 decreased high glucose- induced ROS production. the NADPH activity and the apoptosis rate and the expression level of Rho / ROCK in CMECs, the difference were statistically significant (P <0.05) .Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GL P-1 are dependent on downstream inhibition of Rho through a cAMP / PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.