The water extract of Jagamchotang protects the ischemia/reperfusion-induced cytotoxicity of rat neonatal myocardial cells via generation of nitric oxide

Citation
J. Oh et al., The water extract of Jagamchotang protects the ischemia/reperfusion-induced cytotoxicity of rat neonatal myocardial cells via generation of nitric oxide, IMMUNOPH IM, 22(2), 2000, pp. 297-315
Citations number
21
Categorie Soggetti
Immunology
Journal title
IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
ISSN journal
08923973 → ACNP
Volume
22
Issue
2
Year of publication
2000
Pages
297 - 315
Database
ISI
SICI code
0892-3973(2000)22:2<297:TWEOJP>2.0.ZU;2-1
Abstract
Jagamchotang has been used for treatment of ischemic myocardial diseases in Chinese traditional medicine. However, little is known about the mechanism by which Jagamchotang rescues myocardial cells from ischemic damages. To e lucidate the protective mechanisms, the effects of Jagamchotang on ischemia /reperfusion-induced cytotoxicity and generation of nitric oxide (NO) are i nvestigated in primary neonatal myocardial cells. Ischemia/reperfusion itse lf induces severe myocardial cell death in vitro. However, treatment of the cells with Jagamchotang significantly reduces both ischemia/reperfusion-in duced myocardial cell death and LDH release. In addition, pretreatment of J agamchotang before reperfusion recovers the lose of beating rates after isc hemia/reperfusion. For a while, the water extract of Jagamchotang stimulate s myoardial cells in ischemic condition to produce nitric oxide (NO) in a d ose dependent manner and it protectes the damage of myocardial cells. Furth ermore, the protective effects of the water extract of Jagamchotang is mimi cked by treatment of sodium nitroprusside, an exogenous NO donor. N-G-monom ethyi-L-argine (N(G)MMA), a specific inhibitor of nitric oxide synthase (NO S), significantly blocks the protective effects of Jagamchotang on the cell s after ischemia/reperfusion. Taken together, we suggest that the protectiv e effects of Jagamchotang against ischemia/reperfusion-induced myocardial d amages may be mediated by NO production during ischemic condition.