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KMID : 0385220030130010032
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Korean Journal of Gerontology
2003 Volume.13 No. 1 p.32 ~ p.38
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Nitric Oxide Protects Reactive Oxygen Species-induced Apoptosis in H9C2 Cardiac Muscle Cells
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Chae Han-Jung
Ha Ki-Chan
Jeon Moon-Suk
Yun Dong-Hyeon
Chin Hee-Young
Chae Soo-Wan
Kim Hyung-Ryong
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Abstract
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H2O2-exposed cardiac muscle cells resulted in apoptosis. But the addition of NO donors blocked apoptosis estimated by DNA fragmentation assay, nuclear morphology stained with fluorescent dye, Hoechst 33258. Nitric oxide (NO) reagents, pretreated SNAP and diethylamine nitric oxide (DEANO) attenuates reactive oxygen species (ROS) including hydrogen peroxide (H2O2), menadione or benzenetriol (BT)-mediated injury to H9C2 cardiac muscle cells. Cell permeable PKG inhibitors-ODQ and KT5823, do not have any effect on NO-induced protective effect. The presence of cycloheximide (CHX) or actinomycin D (ACTD) did not reverse NO-induced effect. This confirms that NO protects against cytotoxicity induced by reactive oxygen species (ROS) independently of cGMP as well as protein synthesis. In this study, the amounts of released NO were similar between 4hr-pretreated 100 mM SNAP and 30 mM DEANO. It is suggested that the enough amount of released NO, but less than toxic dose, may be an important factor of the protective effect against ROSinduced apoptosis in H9C2 cardiac muscle cells.
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KEYWORD
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NO, SNAP, DEANO, apoptosis, H9C2 cardiac muscle cells
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