Myricetin blocks lipoteichoic acid-induced COX-2 expression in human gingival fibroblasts
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چکیده
منابع مشابه
Human gingival fibroblasts rescue butyric acid-induced T-cell apoptosis.
We previously demonstrated that butyric acid, an extracellular metabolite from periodontopathic bacteria, induces cytotoxicity and apoptosis in murine thymocytes, splenic T cells, and human Jurkat T cells. In this study, we used a cell-to-cell interaction system to examine the contribution of gingival fibroblasts to the regulation of T-cell death induced by butyric acid. Butyric acid slightly s...
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Cyclooxygenase-2 (COX-2) is continuously expressed in most cancerous cells where it appears to modulate cellular proliferation and apoptosis. However, little is known about the contribution of transient COX-2 induction to cell cycle progression or programmed cell death in primary cells. In this study we determined whether COX-2 regulates proliferation or apoptosis in human fibroblasts. COX-2 mR...
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Lipoteichoic acids (LTA) from various gram-positive bacteria, including oral streptococci such as Streptococcus sanguis, enhanced the production of hepatocyte growth factor (HGF) (scatter factor) by human gingival fibroblasts in culture, whereas lipopolysaccharides (LPS) from various gram-negative bacteria did not. In contrast, LPS induced interleukin 1 activity in human gingival epithelial cel...
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The myofibroblast (MFB) has recently been identified as an important mediator of tumor necrosis factor-α (TNF-α)-associated colitis and cancer, but the mechanism(s) involved remains incompletely understood. Here, we show that treatment of 18Co cells, a model of human colonic MFBs, with TNF-α and lysophosphatidic acid (LPA) induced striking synergistic cyclooxygenase-2 (COX-2) protein expression...
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Introduction Chronic ulcers are an example of abnormal wound healing showing chronic inflammation which can result in delayed healing. One of the reasons that can influence the chronic state of the ulcer edge is a continous state of oxidative stress (1) partially due to a release of toxic metabolites, proteolytic enzymes and toxic free radicals accumulated in the damaged tissue (2). In order to...
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ژورنال
عنوان ژورنال: Cellular and Molecular Biology Letters
سال: 2014
ISSN: 1689-1392
DOI: 10.2478/s11658-014-0186-4