Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose

被引:25
作者
Ge, Guang-Hao [1 ,2 ]
Dou, Hong-Jie [3 ,4 ]
Yang, Shuan-Suo [1 ,2 ]
Ma, Jiang-Wei [1 ,2 ]
Cheng, Wen-Bo [1 ,2 ]
Qiao, Zeng-Yong [1 ,2 ]
Hou, Yue-Mei [1 ,2 ]
Fang, Wei-Yi [5 ]
机构
[1] Fangxian Dist Cent Hosp, Dept Cardiol, Shanghai 201499, Peoples R China
[2] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp South Campus 6, Dept Cardiol, Shanghai 201499, Peoples R China
[3] Fengxian Dist Cent Hosp, Dept Intens Care Unit, Shanghai 201499, Peoples R China
[4] Shanghai Jiao Tong Univ, Affiliated Peoples Hosp South Campus 6, Dept Cardiol, Dept Intens Care Unit, Shanghai 201499, Peoples R China
[5] Shanghai Jiao Tong Univ, Affiliated Chest Hosp, Dept Cardiol, Shanghai 200052, Peoples R China
关键词
Glucagon-like peptid-1; Cardiac microvascular endothelial cell; ROS; Rho/ROCK; OXIDATIVE STRESS; LIRAGLUTIDE PROTECTS; GLP-1; ANALOG; DISEASE; KINASE; COMPLICATIONS; ACTIVATION; PREVENTION; DAMAGE; RISK;
D O I
10.1016/S1995-7645(14)60191-7
中图分类号
R1 [预防医学、卫生学];
学科分类号
100235 [预防医学];
摘要
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.
引用
收藏
页码:73 / 78
页数:6
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