These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Protective effect of glucagon-like peptide-1 analogue on cardiomyocytes injury induced by hypoxia/reoxygenation].
    Author: Liu MM, Shen YF, Chen C, Lai XY, Zhang MY, Yu R.
    Journal: Zhonghua Nei Ke Za Zhi; 2016 Apr 01; 55(4):311-6. PubMed ID: 27030622.
    Abstract:
    OBJECTIVE: To investigate the effect of glucagon-like peptide-1 (GLP-1) receptor agonist liraglutide on hypoxia/reoxygenation (H/R)-induced cardiomyocytes death under high glucose condition and the potential mechanisms. METHODS: H9C2 cardiomyocytes were divided into 4 groups: normal glucose (N, 5 mmol/L), high glucose (G, 20 mmol/L), high glucose in combination with liraglutide (L, 100 nmol/L), high glucose in combination with liraglutide and wortmannin (W, 25 nmol/L). The apoptosis of H9C2 was detected by TUNEL assay. Nitric oxide synthetase(eNOS), nitric oxide (NO) and reactive oxygen(ROS) in supernatants were measured by enzymatic analysis. p-PI3K, PI3K, p-Akt, Akt, Bcl-2, caspase-3 were examined by western blotting. RESULTS: Compared with cells in N group, the apoptosis of H9C2 cells induced by H/R was markedly increased [(15.79±3.92)% vs (9.74±1.14)%, P=0.028] in G group. The same was true for ROS [(489.63±21.01) U/ml vs (338.50±43.60) U/ml, P<0.001] and caspase-3 levels (1.87±0.03 vs 1.15±0.04, P<0.001), but not for Bcl-2 protein expression (1.79±0.06 vs 1.89±0.03, P=0.047). Pretreatment of cells with liraglutide (100 nmol/L) prevented the cell death induced by high glucose and H/R together with decrease of ROS and caspase-3 levels and increase of Bcl-1 expression. Moreover, treatment of cells with liraglutide also significantly increased phosphorylation of PI3K and Akt (p-PI3K/PI3K: 0.87±0.07 vs 0.59±0.09, P=0.002; p-Akt/Akt: 0.34±0.01 vs 0.08±0.01, P<0.001), eNOS[(41.29±0.56)μmpl/L vs (37.20±0.52)μmpl/L, P<0.001)and NO [(31.24±0.40)μmpl/L vs (26.66±0.53)μmpl/L, P<0.001)levels. Furthermore, addition of PI3K/Akt inhibitor wortmanin markedly inhibited the expression of p-PI3K/PI3K, p-Akt/Akt, reversed the changes of eNOS, NO, caspase-3 and Bcl-2 by liraglutide, and abolished the protective effect of liraglutide on cell apoptosis. CONCLUSIONS: GLP-1 receptor agonist liraglutide treatment could alleviate cardiomyocytes apoptosis induced by high glucose and H/R through the activation of PI3K-Akt-eNOS-NO signaling pathway and inhibition of oxidative stress.
    [Abstract] [Full Text] [Related] [New Search]