脂毒素
炎症
白三烯B4
化学
二十烷酸
受体
糖皮质激素受体
脂质信号
药理学
地塞米松
糖皮质激素
甲酰肽受体
白三烯
体内
内分泌学
内科学
花生四烯酸
生物化学
生物
趋化性
医学
酶
生物技术
哮喘
作者
Atsushi Hashimoto,Yousuke Murakami,Hidero Kitasato,Izumi Hayashi,Hirahito Endo
标识
DOI:10.1016/j.biopha.2006.06.023
摘要
Lipoxin A(4) (LXA(4)) is an eicosanoid which is produced via lipoxygenases and characteristic of its anti-inflammatory effect in many metabolites of arachidonic acid, which are mostly pro-inflammatory. Glucocorticoids are well known also for their strong anti-inflammatory action but induce 5-lipoxygenase, essential to synthesize leukotrienes, which are pro-inflammatory. To elucidate the interaction of glucocorticoids and lipoxin A(4) for anti-inflammation, we analyzed in vitro expression of lipoxin A(4) receptor (ALX) on human neutrophils and the in vivo anti-inflammatory effect of glucocorticoids and LXA(4) using a dermal inflammation mouse model. ALX mRNA was up-regulated by dexamethasone (Dex) in human neutrophils. A glucocorticoid receptor antagonist, mifepristone, suppressed up-regulation of ALX induced by Dex. LXA(4) and/or Dex decreased CD11b expression on human neutrophils and suppressed mouse dermatitis induced by LTB(4). These results suggest that anti-inflammatory effects of glucocorticoids depend at least partly on up-regulation of ALX and that the lipoxin system could be a negative feedback regulator for LTB(4).
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