Background Ellagic acid (EA) is a phenolic constituent in fruits and nuts, such as raspberries, strawberries, walnuts, mango kernel and pomegranate. It was documented that EA shows anti-fibrotic, anti-inflammatory activity in vivo model of bowel inflammation and lung fibrosis, however the precise mechanism of signal inhibition was not extensively investigated.
Objectives The objectives of this study are first, to elucidate the anti-inflammatory effect of EA in RAW 264.7 murine macrophage cell line by NF-kB pathway in vitro, and second, to compare it with effect of other immuno-modulating agent, tacrolimus and colchicine.
Methods We determined the cytotoxic effect of EA using MTT assay. The effects of EA on tumor necrosis facor (TNF)-alpha induced mRNA and protein expression were investigated using quantitative real-time PCR and western blot. In addition, we examined the effects of pharmaceutical drugs with anti-inflammatory properties on expression of TNF-alpha.
Results EA significantly suppressed the expression of interleukin-1 beta and TNF-alpha in a dose dependent manner. EA suppressed TNF-alpha induced inflammatory genes expression by inhibiting the phosphorylation of JNK and Akt, whereas had no significant effect on p38 activation. In addition, the inhibitory effect of EA on TNF-alpha induced inflammatory genes expression was regulated by suppression of IkB-alpha phosphorylation and NF-kB translocation. The expression of TNF-alpha mRNA level was reduced comparably treated with EA and other anti-inflammatory agents (ascorbic acid, dexamethasone and colchicine).
Conclusions These findings suggest that EA suppresses inflammatory genes expression through phosphorylation of JNK/Akt and regulation of NF-kB signal pathway in TNF-alpha induced inflammation. Further investigation regarding effects of EA on autoimmune, inflammatory is scheduled.
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Disclosure of Interest None declared
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