Catalase protects cardiomyocytes via its inhibition of nitric oxide synthesis

Nitric oxide (NO) has been reported to play an important role as an effector molecule in cytokine signal transduction in cardiomyocytes. The treatment of IL-1b/ TNF-a (2 ng/ml)/ IFN-g (50 U/ml) induced apoptosis in neonatal rat ventricular cardiomyocytes via NO-dependent pathway. When cardiomyocytes were treated with IL-1b (20 ng/ml)/TNF-a (2 ng/ml)/ IFN-g(50 U/ml) in the presence of catalase, the cells were much more resisant to the cell death as well as NO synthesis. However, catalase significantly enhanced the expression of iNOS protein in cardiomyocytes. (omitted)