Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose
- Author:
Guang-Hao GE
1
;
Shuan-Suo YANG
1
;
Jiang-Wei MA
1
;
Wen-Bo CHENG
1
;
Zeng-Yong QIAO
1
;
Yue-Mei HOU
1
;
Guang-Hao GE
2
;
Shuan-Suo YANG
2
;
Jiang-Wei MA
2
;
Wen-Bo CHENG
2
;
Zeng-Yong QIAO
2
;
Yue-Mei HOU
2
;
Hong-Jie DOU
3
;
Hong-Jie DOU
4
;
Wei-Yi FANG
5
Author Information
- Publication Type:Journal Article
- Keywords: Cardiac microvascular endothelial cell; Glucagon-like peptid-1; Rho/ROCK; ROS
- From: Asian Pacific Journal of Tropical Medicine 2015;8(1):73-78
- CountryChina
- Language:Chinese
- Abstract: 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.
