Abstract
The anti-inflammatory activities of the products of supercritical fluid extraction of Litsea japonica fruit (SFELJF) using supercritical carbon dioxide were investigated. The SFELJF extract dose-dependently inhibited the production of inflammatory markers [nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2), and cyclooxygenase-2 (COX-2)] and proinflammatory cytokines [tumour necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6] induced by lipopolysaccharide (LPS) treatment. To further elucidate the mechanisms underlying these inhibitory effects, LPS-induced nuclear factor-κB (NF-κB) activation and mitogen-activated protein kinase (MAPK) phosphorylation were studied. The SFELJF extract inhibited NF-κB (p65 and p50) activation and MAPK [extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38] phosphorylation in a dose-dependent manner. These results suggest that the anti-inflammatory activities of SFELJF extracts are due to proinflammatory cytokines and mediators via suppression of NF-κB activation and MAPK phosphorylation.
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