Effect of glucagon-like peptide-1 on hypoxia-reoxygenation induced injury in neonatal rat cardiomyocytes.
- 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
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Apoptosis; drug effects; Caspase 3; metabolism; Cell Hypoxia; Cells, Cultured; Glucagon; metabolism; Glucagon-Like Peptide 1; pharmacology; Myocardial Reperfusion Injury; metabolism; Myocytes, Cardiac; drug effects; Rats; Rats, Wistar
- From: Chinese Journal of Cardiology 2010;38(1):72-75
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of glucagon-like peptide-1 (GLP-1) on hypoxia-reoxygenation (H/R) induced injury in neonatal rat cardiomyocytes.
METHODSCultured 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 + UO126 group, H/R + LY294002 group. LDH activity, apoptosis rate of cardiomyocytes, Caspase-3 activity were detected.
RESULTSCompared with normal control group, the activity of LDH, cardiomyocyte apoptosis rate, Caspase-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 Caspase-3 activity (36,809 +/- 4750) RLU vs. (57,602 +/- 9161) RLU, P < 0.01], while LY294002 (PI3K inhibitor) and UO126 (MAPK inhibitor) could block the effects of GLP-1 in cardiomyocytes underwent H/R injury.
CONCLUSIONSGLP-1 could protect H/R injury mainly by inhibiting cardiomyocytes apoptosis via activating PI3K/Akt and MAPK signaling pathway.
