GLP-1 agonist protects myocardial hypoxia-reoxygenation injury through PI3K/ Akt signaling pathway: an experimental study
10.3760/cma.j.issn.1000-6699.2018.01.013
- VernacularTitle:GLP-1激动剂通过PI3K/Akt信号通路减轻心肌细胞缺氧复氧损伤的实验研究
- Author:
Zhigang YI
1
;
Jinhan CHEN
;
Jin LI
;
Wenan GUO
;
Juan WU
;
Shangmeng HUANG
Author Information
1. 361003,厦门大学附属第一医院干部保健病房
- Keywords:
Myocardial ischemia reperfusion injury;
Hypoxia reoxygenation;
Glucagon like peptide 1;
Phosphatidylinositol-3-kinase/ protein kinase B
- From:
Chinese Journal of Endocrinology and Metabolism
2018;34(1):61-66
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of glucagon like peptide 1 (GLP-1) agonist on myocardial hypoxia reoxygenation injury and its molecular mechanism. Methods H9C2 cells were divided into control group, hypoxia reoxygenation(H/ R) group, H/ R+GLP-1 group, and H/ R+GLP-1+phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002 group. The cell proliferation activity, apoptosis rate, enzyme contents in the medium and the expressions of apoptosis-related genes were detected. After animal model of myocardial ischemia reperfusion injury (I/ R) was established and was treated with GLP-1 agonist and PI3K inhibitor, serum enzyme contents were detected. Results Hypoxia reoxygenation decreased the myocardial cell proliferation activity and phosphorylated-PI3K(p-PI3K), phosphorylated-protein kinase B (p-Akt), Bcl-2 protein expressions, increased the apoptotic cell number and creatine kinase ( CK), creatine kinase-MB ( CK-MB), lactate dehydrogenase ( LDH) contents in cell culture medium and Bax, caspase-3 protein expressions, which were ameliorated by GLP-1 ( all P < 0. 05). The myocardial cell proliferation activity and Bcl-2 protein expression of H/ R+GLP-1+LY294002 group were significantly lower than those of H/ R+GLP-1 group while the apoptotic cell number and CK, CK-MB, LDH contents in cell culture medium and Bax, Caspase-3 protein expressions were significantly higher (all P<0. 05). Serum CK, CK-MB, and LDH contents in rats of I/ R group were significantly higher than those in control group and I/ R+GLP-1 group. Serum CK, CK-MB, and LDH contents in rats of I/ R+GLP-1+LY294002 group were significantly higher than those in I/ R+GLP-1 group(all P < 0. 05). Conclusion GLP-1 agonist is able to protect the myocardial hypoxia reoxygenation injury via activating PI3K/ Akt signaling pathway.
