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Wogonin attenuates endotoxin-induced prostaglandin E2 and nitric oxide production via Src-ERK1/2-NFκB pathway in BV-2 microglial cells

Authors

  • Chung-Hsin Yeh,

    1. Department of Neurology, Show Chwan Memorial Hospital, Changhua, Taiwan, Republic of China
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    • These authors contributed equally to this work.

  • Ming-Ling Yang,

    1. Department of Anatomy, School of Medicine, Chung Shan Medical University, Taichung, Taiwan, Republic of China
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    • These authors contributed equally to this work.

  • Chien-Ying Lee,

    1. Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan, Republic of China
    2. Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taiwan, Republic of China
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  • Ching-Ping Yang,

    1. Institute of Microbiology and Immunology, School of Life Science, National Yang-Ming University, Taipei, Taiwan, Republic of China
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  • Yi-Ching Li,

    1. Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taiwan, Republic of China
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  • Chun-Jung Chen,

    1. Department of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan, Republic of China
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  • Yu-Hsiang Kuan

    Corresponding author
    1. Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan, Republic of China
    2. Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taiwan, Republic of China
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Abstract

Microglia are the major component of intrinsic brain immune system in neuroinflammation. Although wogonin expresses anti-inflammatory function in microglia, little is known about the molecular mechanisms of the protective effect of wogonin against microglia activation. The aim of this study was to evaluate how wogonin exerts its anti-inflammatory function in BV2 microglial cells after LPS/INFγ administration. Wogonin not only inhibited LPS/ INFγ-induced PGE2 and NO production without affecting cell viability but also exhibited parallel inhibition on LPS/INFγ-induced expression of iNOS and COX-2 in the same concentration range. While LPS/INFγ-induced expression of P-p65 and P-IκB was inhibited by wogoninonly weak inhibition on P-p38 and P-JNK were observed, whereas it significantly attenuated the P-ERK1/2 and its upstream activators P-MEK1/2 and P-Src in a parallel concentration-dependent manner. These results indicated that the blockade of PGE2 and NO production by wogonin in LPS/INFγ-stimulated BV2 cells is attributed mainly to interference in the Src-MEK1/2-ERK1/2-NFκB-signaling pathway. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1162–1170, 2014.

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