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Research ArticleArticle

Inhibition of Activation of Nuclear Factor κB Is Responsible for Inhibition of Inducible Nitric Oxide Synthase Expression by Higenamine, an Active Component of Aconite Root

Young Jin Kang, Young Soo Lee, Goun Woo Lee, Duck Hyung Lee, Jae Chun Ryu, Hye Sook Yun-Choi and Ki Churl Chang
Journal of Pharmacology and Experimental Therapeutics October 1999, 291 (1) 314-320;
Young Jin Kang
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Young Soo Lee
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Goun Woo Lee
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Duck Hyung Lee
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Jae Chun Ryu
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Hye Sook Yun-Choi
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Ki Churl Chang
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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)-γ. Higenamine concentration-dependently inhibited NO production and inducible NO synthase mRNA in RAW 264.7 cells, in which the IC50 was 53 μM. 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 μg/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 κB in RAW 264.7 cells due to LPS + IFN-γ by mobility shift assays. Taken together, these data strongly suggest that higenamine inhibits iNOS expression by inhibiting nuclear factor κB activation by LPS + IFN-γ, which may be beneficial in inflammatory diseases in which 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.

Footnotes

  • Send reprint requests to: K. C. Chang, Ph.D., Department of Pharmacology, Gyeongsang National University, 92 Chilamdong, Chinju, 660-751, Korea. E-mail: kcchang{at}nongae.gsnu.ac.kr

  • ↵1 Supported by the Korea Research Foundation.

  • Abbreviations:
    LPS
    lipopolysaccharide
    INF
    interferon
    NO
    nitric oxide
    iNOS
    inducible nitric oxide synthase
    NOS
    nitric oxide synthase
    TNF
    tumor necrosis factor
    NF-κB
    nuclear factor κB
    MTT
    3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
    SNP
    sodium nitroprusside
    PMSF
    phenylmethylsulfonyl fluoride
    DTT
    dithiothreitol
    PE
    phenylephrine
    MAP
    mean arterial pressure
    HR
    heart rate
    NE
    norepinephrine
    NOx
    nitrite/nitrate serum level
    RA
    rheumatoid arthritis
    • Received March 18, 1999.
    • Accepted June 17, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 291 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 291, Issue 1
1 Oct 1999
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Research ArticleArticle

Inhibition of Activation of Nuclear Factor κB Is Responsible for Inhibition of Inducible Nitric Oxide Synthase Expression by Higenamine, an Active Component of Aconite Root

Young Jin Kang, Young Soo Lee, Goun Woo Lee, Duck Hyung Lee, Jae Chun Ryu, Hye Sook Yun-Choi and Ki Churl Chang
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 314-320;

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Research ArticleArticle

Inhibition of Activation of Nuclear Factor κB Is Responsible for Inhibition of Inducible Nitric Oxide Synthase Expression by Higenamine, an Active Component of Aconite Root

Young Jin Kang, Young Soo Lee, Goun Woo Lee, Duck Hyung Lee, Jae Chun Ryu, Hye Sook Yun-Choi and Ki Churl Chang
Journal of Pharmacology and Experimental Therapeutics October 1, 1999, 291 (1) 314-320;
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