Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose.
作者信息
Ge Guang-Hao, Dou Hong-Jie, Yang Shuan-Suo, Ma Jiang-Wei, Cheng Wen-Bo, Qiao Zeng-Yong, Hou Yue-Mei, Fang Wei-Yi
机构信息
Department of Cardiology, Fengxian District Central Hospital, Shanghai 201499, China; Department of Cardiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital South campus, Shanghai 201499, China.
Department of Intensive Care Unit, Fengxian District Central Hospital, Shanghai 201499, China; Department of Intensive Care Unit, Department of Cardiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital South campus, Shanghai 201499, China.
出版信息
Asian Pac J Trop Med. 2015 Jan;8(1):73-8. doi: 10.1016/S1995-7645(14)60191-7.
OBJECTIVE
To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose.
METHODS
CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot 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 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.
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