![]() A and B: Effects of quercetin on the viability of normal human gastric mucosa epithelial cells (GES-1). Quercetin suppresses tumor necrosis factor-α-induced matrix metallopeptidase-9 expression in normal human gastric mucosa epithelial cells. GAPDH: Glyceraldehyde-3-phosphate dehydrogenase GES-1: Normal human gastric mucosa epithelial cell line MMP: Matrix metallopeptidase TNF-α: Tumor necrosis factor-α. Data are expressed as the mean ± SEM of three independent experiments. One-way ANOVA was used for comparisons among different treatments ( c P < 0.05, d P < 0.01 vs TNF-α-stimulated cells). One-way ANOVA was used for comparisons among different treatment time points ( a P < 0.05, b P < 0.01 vs control cells in 0 h). The TNF-α antagonist repressed TNF-α-activated MMP-9 expression in GES-1 cells. A: Tumor necrosis factor-α (TNF-α) was used at concentrations of 10, 20, and 30 ng/mL to stimulate normal human gastric mucosa epithelial cells (GES-1) for 0, 16, 20, or 24 h, and matrix metallopeptidase-9 (MMP-9) enzymatic activity was measured by gelatin zymography as described in the Materials and Methods section B: MMP-9 transcripts were analyzed by quantitative reverse transcription-polymerase chain reaction C: Cells were either untreated or treated with a TNF-α antagonist (TNFR inhibitor) (1 mM) 1 h before the addition of TNF-α (30 ng/mL). Tumor necrosis factor-α induces matrix metallopeptidase-9 expression via tumor necrosis factor-α receptor in normal human gastric mucosa epithelial cells. Published by Baishideng Publishing Group Inc. ![]() Quercetin significantly downregulates TNF-α-induced MMP-9 expression in GES-1 cells via the TNFR-c-Src-ERK1/2 and c-Fos or NF-κB pathways.Īnti-inflammatory Matrix metallopeptidase-9 Normal human gastric epithelial cells Quercetin Tumor necrosis factor-α. TNF-α significantly increased GES-1 cell migration, and these results were reduced by pretreatment with quercetin or a TNF-α antagonist. Pretreatment with quercetin, TNF-α antagonist, PP1, U0126, or Bay 11-7082 reduced TNF-α-induced p65 phosphorylation and translocation and p65-Luc activity in a dose- and time-dependent manner. Quercetin, TNF-α antagonist, PP1, U0126, and tanshinone IIA (TSIIA) reduced TNF-α-induced c-Fos phosphorylation and AP-1-Luciferase (Luc) activity in a dose- and time-dependent manner. Quercetin and TNF-α antagonists decreased the TNF-α-induced phosphorylation of c-Src, ERK1/2, c-Fos, and p65 in a dose- and time-dependent manner. These effects were reduced by the pretreatment of GES-1 cells with quercetin or a TNF-α antagonist (TNFR inhibitor) in a dose- and time-dependent manner. QRT-PCR and gelatin zymography showed that TNF-α induced MMP-9 mRNA and protein expression in a dose- and time-dependent manner. MMP-9 mRNA and protein levels were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and gelatin zymography, respectively. p65 expression was detected by immunofluorescence. The expression of proto-oncogene tyrosine-protein kinase Src (c-Src), phospho (p)-c-Src, extracellular-signal-regulated kinase 2 (ERK2), p-ERK1/2, c-Fos, p-c-Fos, nuclear factor kappa B (NF-κB/p65), and p-p65 and the effects of their inhibitors were examined using Western blot analysis and measurement of luciferase activity. Cell migration was measured using Transwell assay. The cell counting Kit-8 assay was used to evaluate the effects of varying quercetin doses on cell viability in the normal GES-1 cell line. The normal human gastric mucosa epithelial cell line GES-1 was used to establish a normal human gastric epithelial cell model of TNF-α-induced MMP-9 protein overexpression to evaluate the anti-inflammatory effects of quercetin. To assess whether tumor necrosis factor-α (TNF-α)-induced MMP-9 expression mediates the anti-inflammatory effects of quercetin in normal human gastric mucosal epithelial cells. However, the effects and mechanisms of action of quercetin on human chronic gastritis and whether quercetin can relieve symptoms remain unclear. ![]() Quercetin and quercetin-rich diets represent potential food supplements and a source of medications for treating gastric injury given their anti-inflammatory activities. Matrix metallopeptidase-9 plays an important role in inflammation and GC progression. Gastric injury is the most common digestive system disease worldwide and involves inflammation, which can lead to gastric ulcer or gastric cancer (GC).
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