Resveratrol reverses D-galactose-induced senescence in cardiomyocytes

AIM: To investigate the effect of resveratrol on aged cardiomyocytes induced by D-galactose and the underlying mechanism. METHODS: Different concentrations of D-galactose (0, 0.1, 1, 10 and 100 g/L) were added into the culture medium for different processing time (0, 12, 24, 48 and 72 h) to induce cardiomyocyte senescence. Cell senescence was indentified by senescence-associated β-galactosidase staining. Cell viability was evaluated by MTT assay. FDG method was used to detect the quantity of β-galactosidase. The establishment of the cardiomyocyte aging model was determined according to the outcome of these detections. After that, different concentrations of resveratrol (2, 10, 50 and 250 μmol/L) were added into the culture medium, and the effect of resveratrol on the aged cardiomyocytes was observed according to the outcome of FDG detection. The activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and the protein level of microtubule-related protein 1 light chain 3 (LC3) in the cells were measured. RESULTS: Compared with control group, the number of β-galactosidase-positive cells in aging group (10 g/L D-galactose exposure for 48 h) was apparently increased. In aging group, the quantity of β-galactosidase detected by FDG was markedly increased, and the activity of SOD was down-regulated while the content of MDA in the cells was increased. The protein level of LC3 II/LC3 I was down-regulated. No significant change of the cell viability between the 2 groups was observed. Compared with aging group, the quantity of β-galactosidase in resveratrol treatment group (at the concentrations of 10 μmol/L and 50 μmol/L) was decreased. Resveratrol also up-regulated the activity of SOD and decreased the content of MDA in the cells. The protein level of LC3 II/LC3 I was up-regulated by resveratrol. CONCLUSION: Activation of oxidative stress and down-regulation of autophagy exist in D-galactose-induced aged cardiomyocytes. Resveratrol attenuates D-galactose-induced senescence in cardiomyocytes.