Open AccessFructus Ligustrum lucidi inhibits inflammatory mediator release through inhibition of nuclear factor‐κB in mouse peritoneal macrophages
Author(s) -
An HyoJin,
Jeong HyunJa,
Um JaeYoung,
Kim HyungMin,
Park YunJum,
Park RaeKil,
Kim EunCheol,
Na HoJeong,
Shin TaeYong,
An HyoJin,
Hong SeungHeon
Publication year - 2007
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1211/jpp.59.9.0013
Subject(s) - lipopolysaccharide , nitric oxide , tumor necrosis factor alpha , inflammation , prostaglandin e , prostaglandin e2 , pharmacology , prostaglandin , chemistry , mechanism of action , endocrinology , medicine , biology , biochemistry , in vitro
ABSTRACT Fructus Ligustrum lucidi (FLL) is a widely used herbal medicine for the treatment of a variety of pathologies. We have investigated the anti‐inflammatory mechanism of FLL in mouse peritoneal macrophages. FLL exerted an anti‐inflammatory action through inhibition of lipopolysaccharide (LPS)‐induced tumour necrosis factor (TNF)‐α production in mouse peritoneal macrophages. The maximal inhibition rate of TNF‐α production by FLL (0.5 mg mL −1 ) was 60.88 + 0.30%. In the inflammatory process, nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) increased in peritoneal macrophages. FLL decreased the protein level of NO and PGE 2 in LPS‐stimulated mouse peritoneal macrophages. In addition, FLL inhibited nuclear factor‐κB activation and IκB‐α degradation by the decrease in IκB‐α phosphorylation. Our study suggested that FLL reduced inflammation via an important molecular mechanism, which might explain its beneficial effect in the regulation of inflammatory reactions.