Melatonin alleviates high glucose-induced primary cardiomyocyte injury via activating the PI3K/p-Akt pathways

  AIM  To investigate the effect of high glucose on cardiomyocytes injury and to verify the effects and mechanisms of melatonin regulating high glucose-induced neonatal mouse primary ventricular myocytes injury.

  METHODS  Neonatal mouse primary ventricular myocytes were cultured in vitro and divided into four groups: normal control group (NG), high glucose group (HG), HG+melatonin group (HG+Mel) and HG+melatonin+PI3k/Akt inhibitor group (HG+Mel+LY294002). Western blotting, RT-PCR and immunofluorescence were used to detect the expressions of apoptosis-associated proteins and the change of PI3K/p-Akt, evaluating the effects and mechanisms of melatonin on high glucose-induced cadiomyocytes apoptosis.

  RESULTS  Compared with NG, the mRNA/protein expressions ofCl-Caspase3 and Caspase9 increased in cardiomyocytes of high glucose group, accompanied with down-regulated mRNA/protein expressions of p-Akt and decreased protein expression of PI3K. Compared with high glucose group, the mRNA/protein expressions of CL-Caspase3 and Caspase9 in cardiomyocytes of HG+Mel group decreased, together with elevated mRNA/protein expressions of p-Akt and increased protein expression of PI3K. Compared with HG+Mel group, the mRNA/protein expressions of CL-Caspase3 and Caspase9 in cardiomyocytes of HG+Mel+LY294002 group increased, together with the decreased mRNA/protein expressions of p-Akt and down-regulated protein expression of PI3K. The results of immunofluorescence were consistent with Western blotting and RT-PCR.

  CONCLUSION  Melatonin alleviates high glucose-induced primary cardiomyocytes injury via activating the PI3K/Akt pathway.