Cardioprotective effects of fucoidan against hypoxia-induced apoptosis in H9c2 cardiomyoblast cells.

CONTEXT

Cardiomyocyte apoptosis plays a critical role in the progress of heart diseases. Fucoidan, a complex-sulfated polysaccharide, has been reported to possess potential cardioprotective efficacy in vivo.

OBJECTIVE

The present study determines whether fucoidan could provide cardioprotection on hypoxia-induced cardiomyocyte apoptosis.

MATERIALS AND METHODS

H9c2 cardiomyoblast cells were incubated with various concentrations (15, 30, and 60 μg/ml) of fucoidan in a humidified incubator at 37 °C with 95% O2 and 5% CO2. After 6 h, hypoxia was processed and the cardioprotective effects of fucoidan were evaluated by applying MTT, ELISA, Hoechst 33258 nucleus staining, and western blot.

RESULTS

Following a 6 h exposure of H9c2 to hypoxic condition, significant reduction was found in cell survival (0.57-fold) and superoxide dismutase (SOD) activity (0.56-fold), which were associated with the increase of malondialdehyde (MDA) level (2.58-fold), creatine phosphokinase (CK, 3.57-fold), and lactate dehydrogenase (LDH) activities (2.39-fold). Moreover, hypoxia-induced apoptosis was confirmed by Hoechst 33258 nuclear staining, and these changes were accompanied by the increase of Bcl-2 (1.27-fold) and Bax expression (2.6-fold). However, preincubation of the cells with fucoidan prior to hypoxia exposure elevated the cell viability (30 μg/ml, 1.18-fold; 60 μg/ml, 1.32-fold) and SOD activity (30 μg/ml, 1.12-fold; 60 μg/ml, 1.25-fold), but decreased the MDA level (30 μg/ml, 0.70-fold; 60 μg/ml, 0.80-fold), CK (30 μg/ml, 0.69-fold; 60 μg/ml, 0.76-fold), and LDH (30 μg/ml, 0.67-fold; 60 μg/ml, 0.86-fold) leakages. Hoechst 33258 nuclear staining observations demonstrated the same protective effect of fucoidan on hypoxia-induced myocardial injury. Also, cardioprotective effects of fucoidan were reflected by increasing Bcl-2 (60 μg/ml, 1.84-fold), as well as decreasing Bax (60 μg/ml, 0.6-fold).

CONCLUSION

Fucoidan had protective effect against hypoxia-induced cardiomyocytes apoptosis, and the mechanism might involve protections of the cell from oxidative injury.