Fucosterol isolated from Undaria pinnatifida inhibits lipopolysaccharide-induced production of nitric oxide and pro-inflammatory cytokines via the inactivation of nuclear factor-?B and p38 mitogen-activated protein kinase in RAW264.7 macrophages.

Fucosterol isolated from Undaria pinnatifida inhibits lipopolysaccharide-induced production of nitric oxide and pro-inflammatory cytokines via the inactivation of nuclear factor-?B and p38 mitogen-activated protein kinase in RAW264.7 macrophages.

Food Chem. 2012 Dec 1;135(3):967-75

Authors: Yoo MS, Shin JS, Choi HE, Cho YW, Bang MH, Baek NI, Lee KT

Abstract
It has been reported that fucosterol has anti-diabetic, anti-oxidant, and anti-osteoporotic effects. We investigated the anti-inflammatory effects and the underlying molecular mechanism of fucosterol in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. Fucosterol suppressed the expressions of inducible nitric oxide synthase (iNOS), tumour necrosis factor-? (TNF-?), and interleukin-6 (IL-6) by downregulating their transcriptions, and subsequently inhibited the productions of nitric oxide, TNF-?, and IL-6. In addition, fucosterol attenuated LPS-induced DNA binding and the transcriptional activity of nuclear factor-?B (NF-?B). These reductions were accompanied by parallel reductions in the phosphorylation and nuclear translocation of NF-?B. Furthermore, fucosterol attenuated the phosphorylations of mitogen-activated protein kinase kinases 3/6 (MKK3/6) and mitogen-activated protein kinase-activated protein kinase 2 (MK2), which are both involved in the p38 MAPK pathway. These results suggest that the anti-inflammatory effects of fucosterol are associated with the suppression of the NF-?B and p38 MAPK pathways.

PMID: 22953812 [PubMed - in process]

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