Open AccessCurcumin attenuates the release of pro‐inflammatory cytokines in lipopolysaccharide‐stimulated BV2 microglia 1
Author(s) -
JIN Chengyun,
LEE Jaedong,
PARK Cheol,
CHOI Yung hyun,
KIM Giyoung
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00651.x
Subject(s) - curcumin , proinflammatory cytokine , microglia , lipopolysaccharide , nitric oxide synthase , nitric oxide , tumor necrosis factor alpha , pharmacology , cytokine , prostaglandin e2 , inflammation , neuroinflammation , chemistry , nf κb , interleukin , signal transduction , immunology , medicine , biochemistry , endocrinology , organic chemistry
Aim: Pro‐inflammatory mediators, such as prostaglandin E 2 (PGE 2 ) and nitric oxide (NO), and pro‐inflammatory cytokines such as interleukin (IL)‐1β, IL‐6, and TNF‐α, play pivotal roles in brain injuries. The anti‐inflammatory properties are known to be associated with significant reductions in pro‐inflammatory mediators in brain injuries. In the present study we investigate whether the effects of curcumin on the production of pro‐inflammatory mediators in lipopolysaccharide (LPS)‐stimulated BV2 microglia. Methods: Curcumin were administered and their effects on LPS‐induced pro‐inflammatory mediators were monitored by Western blotting and RT‐PCR. Result: Curcumin significantly inhibited the release of NO, PGE 2 , and pro‐inflammatory cytokines in a dose‐dependent manner. Curcumin also attenuated the expressions of inducible NO synthase and cyclooxygenase‐2 mRNA and protein levels. Moreover, curcumin suppressed NF‐κB activation via the translocation of p65 into the nucleus. Our data also indicate that curcumin exerts anti‐inflammatory properties by suppressing the transcription of proinflammatory cytokine genes through the NF‐κB signaling pathway. Conclusion: Anti‐inflammatory properties of curcumin may be useful for treating the inflammatory and deleterious effects of microglial activation in response to LPS stimulation.