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Tricin, Flavonoid From Njavara Reduces Inflammatory Responses in hPBMCs by Modulating the p38MAPK and PI3K/Akt Pathways and Prevents Inflammation Associated Endothelial Dysfunction in HUVECs

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dc.contributor.author Shalini, V
dc.contributor.author Chithra, K P
dc.contributor.author Sindhu, G
dc.contributor.author Jayalekshmy, A
dc.contributor.author Helen, A
dc.date.accessioned 2017-07-07T09:49:40Z
dc.date.available 2017-07-07T09:49:40Z
dc.date.issued 2016-02
dc.identifier.citation Immunobiology, 221(2):137-144 en_US
dc.identifier.issn 0171-2985
dc.identifier.uri http://hdl.handle.net/123456789/2835
dc.description.abstract Previous studies revealed the potent anti-inflammatory activity of tricin, the active component of Njavara rice bran. Here, we report the involvement of specific signaling pathways in the protective effect of tricin against LPS induced inflammation in hPBMCs and the role of tricin in modulating endothelial dysfunction in LPS induced HUVECs. Pretreatment with tricin (15 μM) significantly inhibited the release of TNF-α and was comparable to the specific pathway blockers like ERK inhibitor (PD98059), JNK inhibitor (SP600125) and p38 inhibitor (SB203580), whereas an increased release of TNF-α was observed in PI3K/Akt inhibitor (LY294002) treated cells. Tricin alone and combination treatment of tricin and SB203580 showed more significant inhibition of activation of COX-2 and TNF-α than that of SB203580 alone treated group. Combination treatment of tricin and LY294002 showed increased activation of COX-2 and TNF-α, proved that PI3K activation is essential for the anti-inflammatory effect of tricin. Studies conducted on HUVECs revealed the protective effect of tricin against endothelial dysfunction associated with LPS induced inflammation by inhibiting the activation of proinflammatory mediators like TNF-α, IFN-γ, MCP 1 by modulating NF-κB and MAPK signaling pathways. ELISA and flow cytometric analysis again confirmed the protection of tricin against endothelial damage, especially from the decreased activation of cell adhesion molecules like ICAM-1, VCAM-1 and E-Selectin upon tricin treatment. This work establishes the mechanism behind the potent anti-inflammatory activity of the flavonoid tricin. en_US
dc.language.iso en en_US
dc.publisher Elsevier en_US
dc.subject Flavonoid en_US
dc.subject Inflammation en_US
dc.subject Lipopolysaccharide en_US
dc.subject Signaling en_US
dc.subject Tricin en_US
dc.title Tricin, Flavonoid From Njavara Reduces Inflammatory Responses in hPBMCs by Modulating the p38MAPK and PI3K/Akt Pathways and Prevents Inflammation Associated Endothelial Dysfunction in HUVECs en_US
dc.type Article en_US


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