Nicotinamide inhibits inducible nitric oxide synthase mRNA primary rat glial cells

Miki Fujimura; Teiji Tominaga; Takashi Yoshimoto

doi:10.1016/S0304-3940(97)00373-X

Nicotinamide inhibits inducible nitric oxide synthase mRNA primary rat glial cells

Miki Fujimura, Teiji Tominaga, Takashi Yoshimoto

Research output: Contribution to journal › Article › peer-review

16 Citations (Scopus)

Abstract

Nitric oxide (NO) exerts cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of inducible NO synthase (iNOS), enhances neurotoxicity associated with the N-methyl-D- aspartate (NMDA) receptor. The present study examined whether nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, inhibits NO formation in primary culture of rat glial cells. Nicotinamide (5-20 mM) suppressed iNOS mRNA expression and subsequent NO formation, which were induced by the combination of interferon-γ and lipopolysaccharide, in a dose dependent manner. In addition, high-concentration (20 mM) nicotinamide decreased mRNA of interferon regulatory factor-1, a transcription factor which plays a major role in iNOS mRNA induction. These results suggest thai nicotinamide may have protective effect on glial NO-related pathologies by preventing iNOS mRNA induction.

Original language	English
Pages (from-to)	107-110
Number of pages	4
Journal	Neuroscience Letters
Volume	228
Issue number	2
DOIs	https://doi.org/10.1016/S0304-3940(97)00373-X
Publication status	Published - 1997 Jun 6

Keywords

Glial cells
Inducible nitric oxide synthase
Interferon-γ
Lipopolysaccharide
Nicotinamide
Nitric oxide
Nitric oxide synthase
Poly (ADP- ribose) synthetase

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/S0304-3940(97)00373-X

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title = "Nicotinamide inhibits inducible nitric oxide synthase mRNA primary rat glial cells",

abstract = "Nitric oxide (NO) exerts cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of inducible NO synthase (iNOS), enhances neurotoxicity associated with the N-methyl-D- aspartate (NMDA) receptor. The present study examined whether nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, inhibits NO formation in primary culture of rat glial cells. Nicotinamide (5-20 mM) suppressed iNOS mRNA expression and subsequent NO formation, which were induced by the combination of interferon-γ and lipopolysaccharide, in a dose dependent manner. In addition, high-concentration (20 mM) nicotinamide decreased mRNA of interferon regulatory factor-1, a transcription factor which plays a major role in iNOS mRNA induction. These results suggest thai nicotinamide may have protective effect on glial NO-related pathologies by preventing iNOS mRNA induction.",

keywords = "Glial cells, Inducible nitric oxide synthase, Interferon-γ, Lipopolysaccharide, Nicotinamide, Nitric oxide, Nitric oxide synthase, Poly (ADP- ribose) synthetase",

author = "Miki Fujimura and Teiji Tominaga and Takashi Yoshimoto",

year = "1997",

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doi = "10.1016/S0304-3940(97)00373-X",

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T1 - Nicotinamide inhibits inducible nitric oxide synthase mRNA primary rat glial cells

AU - Fujimura, Miki

AU - Tominaga, Teiji

AU - Yoshimoto, Takashi

PY - 1997/6/6

Y1 - 1997/6/6

N2 - Nitric oxide (NO) exerts cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of inducible NO synthase (iNOS), enhances neurotoxicity associated with the N-methyl-D- aspartate (NMDA) receptor. The present study examined whether nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, inhibits NO formation in primary culture of rat glial cells. Nicotinamide (5-20 mM) suppressed iNOS mRNA expression and subsequent NO formation, which were induced by the combination of interferon-γ and lipopolysaccharide, in a dose dependent manner. In addition, high-concentration (20 mM) nicotinamide decreased mRNA of interferon regulatory factor-1, a transcription factor which plays a major role in iNOS mRNA induction. These results suggest thai nicotinamide may have protective effect on glial NO-related pathologies by preventing iNOS mRNA induction.

AB - Nitric oxide (NO) exerts cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of inducible NO synthase (iNOS), enhances neurotoxicity associated with the N-methyl-D- aspartate (NMDA) receptor. The present study examined whether nicotinamide, an inhibitor of poly (ADP-ribose) synthetase, inhibits NO formation in primary culture of rat glial cells. Nicotinamide (5-20 mM) suppressed iNOS mRNA expression and subsequent NO formation, which were induced by the combination of interferon-γ and lipopolysaccharide, in a dose dependent manner. In addition, high-concentration (20 mM) nicotinamide decreased mRNA of interferon regulatory factor-1, a transcription factor which plays a major role in iNOS mRNA induction. These results suggest thai nicotinamide may have protective effect on glial NO-related pathologies by preventing iNOS mRNA induction.

KW - Glial cells

KW - Inducible nitric oxide synthase

KW - Interferon-γ

KW - Lipopolysaccharide

KW - Nicotinamide

KW - Nitric oxide

KW - Nitric oxide synthase

KW - Poly (ADP- ribose) synthetase

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DO - 10.1016/S0304-3940(97)00373-X

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AN - SCOPUS:0030871417

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JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 2

ER -

Nicotinamide inhibits inducible nitric oxide synthase mRNA primary rat glial cells

Abstract

Keywords

ASJC Scopus subject areas

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