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Title 

16α,17α-epoxypregnenolone-20-oxime prevent LPS-induced NO production and iNOS expression in BV-2 microglial cells by inhibiting JNK phosphorylation

Authors 

H N SunM H JinB HanL FengY H HanG N ShenY Z YuC H JinZ X LianD S LeeSun-Uk KimW Z GeY D Cui

Publisher 

Pharmaceutical Society of Japan

Issue Date 

2014

Citation 

Biological & Pharmaceutical Bulletin, vol. 37, no. 7, pp. 1096-1102

Keywords 

MicrogliaNeuroinflammationNitric oxide

Abstract 

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.

ISSN 

0918-6158

Link 

http://dx.doi.org/10.1248/bpb.b13-00706

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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