대한약학회:학술대회논문집 (Proceedings of the PSK Conference)
- 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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- Pages.80.3-81
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- 2003
Catalase protects cardiomyocytes via its inhibition of nitric oxide synthesis
- Chae, Han-Jung (Laboratory of Pharmacology College of Medicine, Chonbuk National University) ;
- Chae, Soo-Wan (Laboratory of Pharmacology College of Dentistry, Wonkwangk University) ;
- Kim, Hyung-Ryong (Laboratory of Pharmacology College of Dentistry, Wonkwangk University)
- 발행 : 2003.10.01
초록
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)
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