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Molecular mechanisms of anti-inflammatory action of the flavonoid, tricin from Njavara rice (Oryza sativa L.) in human peripheral blood mononuclear cells: possible role in the inflammatory signaling

, : Molecular mechanisms of anti-inflammatory action of the flavonoid, tricin from Njavara rice (Oryza sativa L.) in human peripheral blood mononuclear cells: possible role in the inflammatory signaling. International Immunopharmacology 14(1): 32-38

Flavonoids are a group of natural substances that are located in sources of vegetal origin and are able to regulate acute and chronic inflammatory responses. The anti-oxidant and anti-inflammatory effects corroborate with the preferential use of Njavara, a rice variety in indigenous medicine and the phytochemical investigations revealed the occurrence of a flavonoid, tricin at significantly higher levels compared to staple varieties. This study describes the new aspects of inflammatory suppression by the Njavara rice by evaluating the role of active constituent, tricin in the regulation of production of various pro?inflammatory markers by human peripheral blood mononuclear cells stimulated with lipopolysaccharide. Treatment with tricin resulted in significant down?regulation of LPS-elicited production of TNF-?, IL-6, PGE2 and NO. Tricin was found to be a potential blocker of the expression of isoforms of nitric oxide synthase, cyclooxygenase and matrix metalloproteinases. Modulation of the cascade of molecular events in lipopolysaccharide signaling also includes inhibition of transcription factor NF-?B evidenced by the detection of enhanced p65 subunit in the nuclear extracts on tricin supplementation. The present study summarizes the role of the flavonoid, tricin in the modulation of the expression of different inflammatory mediators and revealed that the inhibitory effects on cell signaling pathways are responsible for its anti-inflammatory activity. Human peripheral blood mononuclear cells were used as the model system for evaluating the effect of tricin. Tricin inhibited the LPS induced release of cytokines from the mononuclear cells. Tricin prevented the overexpression of pro?inflammatory enzymes. Tricin modulated the inflammatory signaling cascade by blocking the activation of nuclear factor ?B.


PMID: 22705359

DOI: 10.1016/j.intimp.2012.06.005

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