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Article Publish Status: FREE
Abstract Title:

Quercetin Inhibits Inflammatory Response Induced by LPSin Human Gingival Fibroblasts via Suppressing NF-B Signaling Pathway.

Abstract Source:

Biomed Res Int. 2019 ;2019:6282635. Epub 2019 Aug 20. PMID: 31531360

Abstract Author(s):

Gang Xiong, Wansheng Ji, Fei Wang, Fengxiang Zhang, Peng Xue, Min Cheng, Yanshun Sun, Xia Wang, Tianliang Zhang

Article Affiliation:

Gang Xiong

Abstract:

Quercetin, a natural flavonol existing in many food resources, has been reported to be an effective antimicrobial and anti-inflammatory agent for restricting the inflammation in periodontitis. In this study, we aimed to investigate the anti-inflammatory effects of quercetin on() lipopolysaccharide- (LPS-) stimulated human gingival fibroblasts (HGFs). HGFs were pretreated with quercetin prior to LPS stimulation. Cell viability was evaluated by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of inflammatory cytokines, including interleukin-1(IL-1), interleukin-6 (IL-6), and tumor necrosis factor-(TNF-), along with chemokine interleukin-8 (IL-8), were determined by enzyme-linked immunosorbent assay (ELISA). The mRNA levels of IL-1, IL-6, IL-8, TNF-, IB, p65 subunit of nuclear factor-kappa B (NF-B), peroxisome proliferator-activated receptor-(PPAR-), liver X receptor(LXR), and Toll-like receptor 4 (TLR4) were measured by real-time quantitative PCR (RT-qPCR). The protein levels of IB, p-IB, p65, p-p65, PPAR-, LXR, and TLR4 were characterized by Western blotting. Our results demonstrated that quercetin inhibited the LPS-induced production of IL-1, IL-6, IL-8, and TNF-in a dose-dependent manner. It also suppressed LPS-induced NF-B activation mediated by TLR4. Moreover, the anti-inflammatory effects of quercetin were reversed by the PPAR-antagonist of GW9662. In conclusion, these results suggested that quercetin attenuated the production of IL-1, IL-6, IL-8, and TNF-inLPS-treated HGFs by activating PPAR-which subsequently suppressed the activation of NF-B.

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