Quercetin 3,7-O-dimethyl ether from Siegesbeckia pubescens suppress the production of inflammatory mediators in lipopolysaccharide-induced macrophages and colon epithelial cells

Abstract

Siegesbeckia pubescens (Compositae) is an annual herb indigenous to Korean mountainous regions. Recent reports have been issued on some compounds derived from S. pubescens for its anti-inflammatory activity or mode of action. The quercetin 3,7-O-dimethyl ether (QDE) isolated from the herbs of S. pubescens suppressed the lipopolysaccharide (LPS)-induced nitric oxide and inducible nitric oxide synthase (iNOS) protein production in mouse macrophages. QDE downregulated pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, tumor necrosis factor -α levels in LPS-stimulated macrophages. Also, QDE decreased the expression of LPS-induced iNOS and cyclooxygenase-2 (COX-2) protein and the production of IL-8 in LPS-induced HT-29 cells. Macrophages and colon epithelial cells are important for regulating the colon immune systems, thus QDE may regulate inflammatory colon disease via LPS-induced inflammation in macrophages and colon epithelial cells. QDE, anti-inflammatory constituent of S. pubescens herbs, can be expected to be a potential candidate for therapeutics against inflammatory bowel disease.

Triterpenoids Isolated from <i>Alnus japonica</i> Inhibited LPS-Induced Inflammatory Mediators in HT-29 Cells and RAW264.7 Cells

“…Expression of Pro-inflammatory Cytokines 14) The level of IL-8 was determined using enzyme-linked immunosorbent assay (ELISA) kits (BD OptEIA , CA, U.S.A.) in HT-29 human colonic epithelial cells. The levels of IL-1β and IL-6 were detected by mouse ELISA kits (Cusabio, Wuhan, China) in RAW264.7 mouse macrophage cells.…”

Onion bulb extract can both reverse and prevent colitis in mice via inhibition of pro-inflammatory signaling molecules and neutrophil activity

“…Various pro-inflammatory signaling molecules were shown to play a role in colitis pathogenesis. For example, enhanced expression/activity profile of the MAPK family members (p38 MAPK, JNK, and ERK1/2) [ 27 , 46 ], PI3K [ 47 , 48 ], and the pro-inflammatory COX-2 [ 49 – 52 ] was observed in the colonic biopsies of IBD patients as well as in different animal models of colitis [ 25 ]. In addition, using chemical inhibitors of these pro-inflammatory molecules ameliorated colitis severity.…”

Luteolin, quercetin, genistein and quercetagetin inhibit the effects of lipopolysaccharide obtained from Porphyromonas gingivalis in H9c2 cardiomyoblasts

“…Various studies have shown that they possess anti-inflammatory properties. Luteolin, genistein, quercetin and quercetagetin inhibited LPS-induced expression of inflammatory mediators such as TNFα and NO by suppressing NF-κB activation [ 22 – 24 ]. Furthermore, these flavonoids exerted inhibitory effects on IkB degradation.…”

“…However, we found no effect of quercetin on COX-2 expression. We also reported that luteolin inhibited nuclear localization and transcriptional activation of NF-κB [ 24 ].…”

“…Quercetin (3,3′,4′,5,7-pentahydroxyflavanone) is a flavonol that displays protective effects against oxidative stress-induced cardiomyoblast apoptosis [ 20 – 22 ]. Quercetin inhibits LPS-induced TNF-α production in macrophages [ 23 ] in additon to LPS-induced IL-8 production in A549 lung cells [ 24 ]. Quercetin can inhibit LPS-induced mRNA levels of COX-2, reducing apoptotic neuronal cell death caused by microglial activation [ 25 ].…”