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Titolo:
Inhibition of activation of nuclear factor kappa B is responsible for inhibition of inducible nitric oxide synthase expression by higenamine, an active component of aconite root
Autore:
Kang, YJ; Lee, YS; Lee, GW; Lee, DH; Ryu, JC; Choi, HSY; Chang, KC;
Indirizzi:
Gyeongsang Natl Univ, Dept Pharmacol, Coll Med, Chinju 660751, South KoreaGyeongsang Natl Univ Chinju South Korea 660751 hinju 660751, South Korea Gyeongsang Natl Univ, Cardiovasc Res Inst, Coll Med, Chinju 660751, South Korea Gyeongsang Natl Univ Chinju South Korea 660751 hinju 660751, South Korea Sogang Univ, Dept Chem, Seoul 121742, South Korea Sogang Univ Seoul South Korea 121742 ept Chem, Seoul 121742, South Korea Seoul Natl Univ, Inst Nat Prod Res, Seoul, South Korea Seoul Natl Univ Seoul South Korea Inst Nat Prod Res, Seoul, South Korea Inst Sci & Technol, Seoul, South Korea Inst Sci & Technol Seoul South Korea Sci & Technol, Seoul, South Korea
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 1, volume: 291, anno: 1999,
pagine: 314 - 320
SICI:
0022-3565(199910)291:1<314:IOAONF>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
SEPTIC SHOCK; L-ARGININE; BISBENZYLISOQUINOLINE ALKALOIDS; MYOCARDIAL DEPRESSION; SMOOTH-MUSCLE; NO SYNTHASE; RAT; MACROPHAGES; INDUCTION; ENDOTOXIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Chang, KC Gyeongsang Natl Univ, Dept Pharmacol, Coll Med, 92 Chilamdong, Chinju 660751, South Korea Gyeongsang Natl Univ 92 Chilamdong Chinju South Korea 660751 ea
Citazione:
Y.J. Kang et al., "Inhibition of activation of nuclear factor kappa B is responsible for inhibition of inducible nitric oxide synthase expression by higenamine, an active component of aconite root", J PHARM EXP, 291(1), 1999, pp. 314-320

Abstract

Effects of higenamine on nitric oxide (NO) production and inducible NO synthase (iNOS) mRNA expression (RAW 264.7 cells), on vascular reactivity in vitro and in vivo (rats), and on survival rates (mice) and serum nitrite/nitrate levels (rats) were investigated by using last lipopolysaccharide (LPS)plus interferon (IFN)-gamma. Higenamine concentration-dependently inhibited NO production and inducible NO synthase mRNA in RAW 264.7 cells, in whichthe IC50 was 53 mu M. Higenamine (10 mg/kg i.p.) administered 90 min before LPS (5 mg/kg i.v.) prevented not only LPS-induced hypotension but also pressor response to norepinephrine (1 mg/kg) in rats. Incubation of thoracic aorta with LPS (300 ng/ml) for 8 h in vitro resulted in suppression of the vasoconstrictor effects to phenylephrine, which was prevented by coincubation with higenamine. The survival rate to endotoxin in mice was significantly (P<.01) increased by the presence of higenamine in the LPS-treated group up to 48 h. Serum nitrite/nitrate levels were significantly (P <.05) reduced by higenamine in LPS-treated rats. Finally, higenamine inhibited the activation of nuclear factor kappa B in RAW 264.7 cells due to LPS + IFN-gamma by mobility shift assays. Taken together, these data strongly suggest that higenamine inhibits iNOS expression by inhibiting nuclear factor kB activation by LPS + IFN-gamma, which may be beneficial in inflammatory diseases inwhich enhanced formation of NO is the main causative factor. Furthermore, due to positive inotropic action, higenamine may be more effective in a condition where myocardial contractility is likely to depress, such as in septic shock and/or endotoxin-induced inflammatory disorders.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 11:16:03