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Myricetin suppresses lipoteichoic acid‐induced interleukin‐1β and cyclooxygenase‐2 expression in human gingival fibroblasts
Author(s) -
GutiérrezVenegas Gloria,
Luna Oscar Alonso,
VenturaArroyo Jairo Agustín,
HernándezBermúdez Cristina
Publication year - 2013
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12103
Subject(s) - myricetin , lipoteichoic acid , pharmacology , biology , cyclooxygenase , proinflammatory cytokine , periodontitis , viability assay , connective tissue , flavones , cytokine , biochemistry , flavonoid , inflammation , immunology , enzyme , cell , medicine , antioxidant , genetics , botany , bacteria , staphylococcus aureus , kaempferol
Periodontitis is an inflammatory disease affecting the connective tissue and supporting bone surrounding the teeth. In periodontitis, human gingival fibroblasts (HGFs) synthesize IL‐1β, causing a progressive inflammatory response. Flavones demonstrate a variety of biological activity: among others, they possess anti‐inflammatory properties. Myricetin is a flavone with a strong anti‐inflammatory activity. The objective of this study was to evaluate the effect of the flavonoid myricetin on HGFs under inflammatory conditions induced by lipoteichoic acid (LTA). the effect of myricetin on HGFs was assessed by measuring cell viability, signaling pathways and IL‐1β expression and synthesis. It was found that, over time, myricetin did not affect cell viability. However, it inhibited activation of p38 and extracellular‐signal‐regulated kinase‐1/2 in LTA‐treated HGFs and also blocked IκB degradation and cyclooxygenase‐2 and prostaglandin E2 synthesis and expression. These findings suggest that myricetin has therapeutic effects in the form of controlling LTA‐induced inflammatory responses.