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The effects of Kolaviron, a Natural Flavonoid from the Seeds of Garcinia Kola on LPS‐induced Inflammation in Macrophages
Author(s) -
Abarikwu sunny
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.716.2
Subject(s) - p38 mitogen activated protein kinases , phosphorylation , chemistry , nf κb , iκbα , protein kinase b , creb , lipopolysaccharide , garcinia kola , pharmacology , inflammation , signal transduction , biology , biochemistry , mapk/erk pathway , transcription factor , immunology , gene , microbiology and biotechnology
Kolaviron (Kol‐v), an important component of Garcinia kola seed has a variety of biologic activities, including anti‐inflammatory properties. In this study, we investigated the possible anti‐inflammatory effect of Kol‐v against pro‐inflammatory responses induced by LPS and the associated signalling pathways in vitro . The protective effects of Kol‐v were determined by measuring gene expressions and activation of inflammatory molecules in LPS‐activated RAW macrophages. We found that Kol‐v inhibited LPS‐induced phosphorylation of p‐c‐JUN and p38 but not IκBα, NF‐κB (p65), ERK1/2, JNK, and IκBα degradation. Kol‐v also suppressed LPS‐induced IL‐18 and LPS‐down‐regulated IP‐10 gene expressions but had no effect on the LPS‐induced gene expression levels of IL‐1α, IL‐33, IL‐1β, IFNβ1‐1, and TNF‐α. Kol‐v concentrations (50 and 100 μM), blocked the phosphorylation of Akt, ERK1/2, IκBα, p38, and NF‐κB but not CREB. The protective effect on JNK phosphorylation was observed at 100 μM Kol‐v. At all concentrations of Kol‐v (10‐100 μM) tested, Kol‐v suppressed the production of IL‐6 in a concentration dependent manner but had no effect on LPS‐induced secretion of TNF‐α. Collectively, these results suggest that Kol‐v interferes with LPS signalling by reducing the activation of several inflammatory transcription factors and that its inhibitory action on IL‐6 secretion correlates with inhibition of ERK1/2, p38, Akt, p‐c‐JUN and JNK signalling pathways.