16α,17α-Epoxypregnenolone-20-oxime Prevent LPS-Induced NO Production and iNOS Expression in BV-2 Microglial Cells by Inhibiting JNK Phosphorylation

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  • Sun Hu-Nan
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Jin Mei-Hua
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Han Bing
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Feng Li
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Han Ying-Hao
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Shen Gui-Nan
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Yu Yong-Zhong
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Jin Cheng-Hao
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Lian Zheng-Xing
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Lee Dong-Soek
    School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University
  • Kim Sun-Uk
    National Primate Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB)
  • Ge Wen-Zhong
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University
  • Cui Yu-Dong
    College of Life Science & Biotechnology, Heilongjiang Bayi Agricultural University

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The free radical nitric oxide (NO), a main member of neuroinflammatory cytokine and a gaseous molecule produced by activated microglia, has many physiological functions, including neuroinflammation. In the present study, we evaluated the effects of serial 16-dehydropregnenolone-3-acetate derivatives on lipopolysaccharide (LPS)-induced NO production and inducible nitric oxide synthase (iNOS) expression in BV-2 microglial cells. Among the six derivatives tested, the increases in NO production and iNOS expression observed in BV-2 microglial cells after LPS stimulation were significantly inhibited by treatment with 16α, 17α-epoxypregnenolone-20-oxime. Moreover, the inhibitory effect of 16α,17α-epoxypregnenolone-20-oxime on NO production was similar to that of S-methylisothiourea sulfate (SMT), an iNOS inhibitor. Further studies showed that 16α,17α-epoxypregnenolone-20-oxime inhibited c-Jun N-terminal kinase (JNK) phosphorylation but not inhibitor kappa B (IκB)-α degradation. Our data in LPS-stimulated microglia cells suggest that 16α,17α-epoxypregnenolone-20-oxime might be a candidate therapeutic for treatment of NO induced neuroinflammation and could be a novel iNOS inhibitor.

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