Effect of glucagon-like deptide-1 on hypoxia-reoxygenation induced injury in neonatal rat cardiomyocytes
10.3760/cma.j.issn.0253-3758.2010.01.019
- VernacularTitle:胰高血糖素样肽1对乳鼠心肌细胞凋亡的影响及其机制
- Author:
Shao-Xin WANG
1
;
Yun XIE
;
Xue ZHOU
;
Wei-Wei SHA
;
Wei-Lin WANG
;
Li-Ping HAN
;
Jia-Chi WANG
;
De-Min YU
Author Information
1. 天津医科大学代谢病医院
- Keywords:
Myocytes,cardiac;
Glucngon-like peptide 1;
Apoptosis;
Hypoxia reoxygenation
- From:
Chinese Journal of Cardiology
2010;38(1):72-75
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes. Methods Cultured neonatal rat cardiomyocytes were randomly divided into seven groups: normal control group, H/R group, GLP-1 + H/R group, GLP-1 + H/R + UO126 group, GLP-1 + H/R + LY294002 group, H/R + U0126 group, H/R +LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected. Results Compared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspsse-3 activity were all significantly increased in H/R group (all P <0.01). However, compared with H/R group, these changes were significantly attenuated in GLP-1 + H/R group [the activity of LDH (128.47±7.96) U/L vs. (223.96±22.10) U/L, P < 0.01, and cardiomyocyte apoptosis rate (2.84±2.56)% vs. (12.58±6.69) %, P < 0.01, and Caspsse-3 activity (36 809±4750) RLU vs. (57 602±9161) RLU, P < 0.01], while LY294002 (PBK inhibitor) and U0126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury. Conclusions GLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.
