非西汀
活力测定
MAPK/ERK通路
p38丝裂原活化蛋白激酶
牙龈卟啉单胞菌
脂多糖
化学
激酶
前列腺素E2
蛋白激酶A
污渍
药理学
细胞
分子生物学
生物化学
牙周炎
免疫学
生物
医学
类黄酮
内科学
抗氧化剂
基因
作者
Gloria Gutiérrez‐Venegas,Anabel Contreras-Sánchez,Jairo Agustín Ventura‐Arroyo
标识
DOI:10.1080/10286020.2014.932351
摘要
Fisetin is an anti-inflammatory flavonoid; however, its anti-inflammatory mechanism is not yet understood. In this study, we evaluated the anti-inflammatory effect of fisetin and its association with mitogen-activated protein kinase (MAPK) and nuclear factor kappa-beta pathways in human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) obtained from Porphyromonas gingivalis. The cell signaling, cell viability, and cyclooxygenase-2 (COX-2) expression of HGFs treated with various concentrations (0, 1, 5, 10, and 15 μM) of fisetin were measured by cell viability assay (MTT), Western blotting, and reverse transcriptase polymerase chain reaction analysis on COX-2. We found that fisetin significantly reduced the synthesis and expression of prostaglandin E2 in HGFs treated with LPS. Activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38 MAPK was suppressed consistently by fisetin in HGFs treated with LPS. The data indicate that fisetin inhibits MAPK activation and COX-2 expression without affecting cell viability. These findings may be valuable for understanding the mechanism of the effect of fisetin on periodontal disease.
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