ABSTRACT
To study the possible mechanism of the effect of glucagon-like peptide-1 (GLP-1) on injury to neonatal rat cardiomyocytes induced by hypoxia-reoxygenation. Lactate dehydrogenase activity [(210.0±11.5) vs (101.4±6.5) U/L] ,apoptosis rate [(8. 138±1. 512) vs(0. 575±0. 168)%] ,and caspase-3 activity [(44.52± 5.69)vs(19.98±1.97) ,all P<0.01] were all increased after hypoxia-reoxygenation. GLP-1 appears to directly act on cardiomyocytes and to protect them from hypoxia-reoxygenation injury [lactate dehydrogenase (190.2±9.0) U/ L, apoptosis rate (2.688±0.580) %, caspase-3 activity 30.34±4.18] mainly by inhibiting the apoptosis probably via the PBK/Akt signaling pathways.
ABSTRACT
Glucagon-like poptide-1 (GLP-1) is an incretin secreted by the enteroendocrine L cells of the gut. Upon the activation of GLP-1 receptor, adenylyl cyclase is activated and cAMP is generated, leading to the activation of protein kinase A and Epac signal pathway. GLP-1 could also activate calcium/calmodulin pathway as well as mitogen-activated protein kinases and phosphatidyl inositol-3 kinase pathway. GLP-1 not only stimulates the phase 1 and phase 2 insulin secretion, but also increases insulin synthesis. GLP-1 also stimulates proliferation and differentiation of islet β-cells, and protects β-cell from apoptosis and modulates endoplasmic reticulum stress response leading to promotion of β-cell adaptation and survival.