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• W2015410009 abstract "ObjectiveTo determine the levels of COX-1, COX-2, and prostaglandin (PG) E2 in human fibroblasts isolated from normal peritoneal and adhesion tissues.DesignProspective experimental study.SettingUniversity medical center.Patient(s)Fibroblast cultures from both peritoneum and adhesion tissues of five patients.Intervention(s)Treatment of the primary cultured fibroblasts with NS398.Main Outcome Measure(s)We used Western blot to determine the effects of hypoxia on COX-1 and COX-2 levels from lysates of normal peritoneal and adhesion fibroblasts before and after hypoxia. We also used the ELISA techniques to determine PGE2 levels in media collected from these fibroblasts before and after hypoxia and with and without NS398, a COX-2–specific inhibitor.Result(s)There was no difference in COX-1 levels between normal and adhesion fibroblasts with and without hypoxia. Basal COX-2 and PGE2 levels were significantly higher in adhesion than normal fibroblasts. Hypoxia gradually increased COX-2 and PGE2 levels in normal peritoneal fibroblasts over time, reaching a peak at 24 hours but had no effect on adhesion fibroblasts. Inhibition of COX-2 by NS398 significantly reduced PGE2 levels in both normal and adhesion fibroblasts.Conclusion(s)The presence of higher levels of COX-2 in adhesion fibroblasts and the induction of COX-2 in normal peritoneal fibroblasts in response to hypoxia indicate a possible inflammatory response. Regulation of COX-2 may alter peritoneal healing and may provide the opportunity to reduce postoperative adhesion development. To determine the levels of COX-1, COX-2, and prostaglandin (PG) E2 in human fibroblasts isolated from normal peritoneal and adhesion tissues. Prospective experimental study. University medical center. Fibroblast cultures from both peritoneum and adhesion tissues of five patients. Treatment of the primary cultured fibroblasts with NS398. We used Western blot to determine the effects of hypoxia on COX-1 and COX-2 levels from lysates of normal peritoneal and adhesion fibroblasts before and after hypoxia. We also used the ELISA techniques to determine PGE2 levels in media collected from these fibroblasts before and after hypoxia and with and without NS398, a COX-2–specific inhibitor. There was no difference in COX-1 levels between normal and adhesion fibroblasts with and without hypoxia. Basal COX-2 and PGE2 levels were significantly higher in adhesion than normal fibroblasts. Hypoxia gradually increased COX-2 and PGE2 levels in normal peritoneal fibroblasts over time, reaching a peak at 24 hours but had no effect on adhesion fibroblasts. Inhibition of COX-2 by NS398 significantly reduced PGE2 levels in both normal and adhesion fibroblasts. The presence of higher levels of COX-2 in adhesion fibroblasts and the induction of COX-2 in normal peritoneal fibroblasts in response to hypoxia indicate a possible inflammatory response. Regulation of COX-2 may alter peritoneal healing and may provide the opportunity to reduce postoperative adhesion development." @default.
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• W2015410009 date "2005-04-01" @default.
• W2015410009 modified "2023-10-09" @default.
• W2015410009 title "Hypoxia upregulates cyclooxygenase-2 and prostaglandin E2 levels in human peritoneal fibroblasts" @default.
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• W2015410009 doi "https://doi.org/10.1016/j.fertnstert.2004.11.037" @default.
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