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Research ArticleCELLULAR AND MOLECULAR

Flavonoid Baicalein Attenuates Activation-Induced Cell Death of Brain Microglia

Kyoungho Suk, Heasuk Lee, Sang Soo Kang, Gyeong Jae Cho and Wan Sung Choi
Journal of Pharmacology and Experimental Therapeutics May 2003, 305 (2) 638-645; DOI: https://doi.org/10.1124/jpet.102.047373
Kyoungho Suk
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Heasuk Lee
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Sang Soo Kang
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Gyeong Jae Cho
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Wan Sung Choi
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Abstract

Baicalein (5,6,7-trihydroxyflavone), a flavonoid originated from the root of Chinese medicinal herb Scutellaria baicalensis, has been shown to exert anti-inflammatory and antioxidant effects, and it is a well known inhibitor of 12-lipoxygenase. We have previously reported that neuroglia undergo nitric oxide (NO)-dependent and NO-independent apoptosis upon inflammatory activation. In the current work, we asked how anti-inflammatory baicalein influences autoregulatory apoptosis of activated microglia and their NO production. Baicalein attenuated NO production and apoptosis of lipopolysaccharide (LPS)-activated, but not interferon-γ-activated, BV-2 mouse microglial cells as well as rat primary microglia cultures. The inhibition of NO production by baicalein was due to the suppression of inducible NO synthase induction. Moreover, baicalein inhibited LPS-induced nuclear factor-κB (NF-κB) activity in BV-2 cells without affecting caspase-11 activation, interferon regulatory factor-1 induction, or signal transducer and activator of transcription-1 phosphorylation. Transfection of BV-2 cells with a p65 subunit of NF-κB abolished the apoptosis-attenuating effects of baicalein, indicating that the inhibition of NF-κB is a major mechanism of action. Baicalein, however, did not significantly affect NO donor-mediated cytotoxicity, and the apoptosis-attenuating effects of baicalein were independent of 12-lipoxygenase inhibition. Based on our previous findings that activation-induced cell death (AICD) of microglia occurs through two separate pathways (NO-dependent pathway and caspase-11-dependent pathway), our current results suggest that baicalein selectively inhibits the NO-dependent apoptotic pathway of activated microglia by suppressing cytotoxic NO production. Also, the AICD-inhibiting effects of baicalein were specific for the inflammatory stimulus that activated microglia.

Footnotes

  • This work was supported by grants to K.S. from the Korea Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (01-PJ8-PG3-21304-0005).

  • DOI: 10.1124/jpet.102.047373

  • Abbreviations:
    LPS
    lipopolysaccharide
    NO
    nitric oxide
    CNS
    central nervous system
    IFNγ
    interferon-γ
    AICD
    activation-induced cell death
    NMMA
    N-monomethyll-arginine
    SNAP
    S-nitroso-N-acetylpenicillamine
    NAC
    N-acetyl cysteine
    z-VAD-fmk
    z-Val-Ala-Asp(OMe)-CH2F
    Ac-LEHD-AFC
    Ac-Leu-Glu-His-Asp-7-amino-4-trifluoromethyl coumarin
    12(S)-HETE
    12-hydroxyeicosatetraenoic acid
    MTT
    3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide
    ECL
    enhanced chemiluminescence
    NOS
    nitric-oxide synthase
    iNOS
    inducible NOS
    STAT1
    signal transducer and activator of transcription 1
    NF-κB
    nuclear factor-κB
    IRF-1
    interferon regulatory factor 1
    RT-PCR
    reverse transcription-polymerase chain reaction
    • Received November 26, 2002.
    • Accepted January 6, 2003.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 305 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 305, Issue 2
1 May 2003
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Research ArticleCELLULAR AND MOLECULAR

Flavonoid Baicalein Attenuates Activation-Induced Cell Death of Brain Microglia

Kyoungho Suk, Heasuk Lee, Sang Soo Kang, Gyeong Jae Cho and Wan Sung Choi
Journal of Pharmacology and Experimental Therapeutics May 1, 2003, 305 (2) 638-645; DOI: https://doi.org/10.1124/jpet.102.047373

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Research ArticleCELLULAR AND MOLECULAR

Flavonoid Baicalein Attenuates Activation-Induced Cell Death of Brain Microglia

Kyoungho Suk, Heasuk Lee, Sang Soo Kang, Gyeong Jae Cho and Wan Sung Choi
Journal of Pharmacology and Experimental Therapeutics May 1, 2003, 305 (2) 638-645; DOI: https://doi.org/10.1124/jpet.102.047373
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