Effects of short-chain acyl-CoA dehydrogenase on cardiomyocyte apoptosis

AIM: To investigate the change of short-chain acyl-CoA dehydrogenase(SCAD) expression during cardiomyocyte apoptosis and to explore the relationship between SCAD and cardiomyocyte apoptosis.METHODS: The neonatal rat cardiomyocytes treated by tert-butyl hydroperoxide(tBHP) were used as the model of cardiomyocyte apoptosis. The cell viability, the expression of SCAD at mRNA and protein levels, the activity of SCAD and the content of free fatty acids were determined.RESULTS: The mRNA and protein expression of SCAD decreased in the cardiomyocyte apoptosis model. Compared with negative control group, SCAD expression and activity were both significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the cardiomyocytes. Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP.CONCLUSION: Down-regulation of SCAD may play an important role in primary cardiomyocyte apoptosis. Increase in the expression of SCAD may become an important part in intervening cardiomyocyte apoptosis.