Inhibition of both COX-1 and COX-2 and resulting decrease in the level of prostaglandins E2 is responsible for non-steroidal anti-inflammatory drug (NSAID)-dependent exacerbation of colitis

Activation of the aryl hydrocarbon receptor pathway may ameliorate dextran sodium sulfate‐induced colitis in mice

“…9 A strong systemic activation of the AhR pathway is observed at 7 days after the TCDD administration in mice. 10 On the basis of that study, mice were pretreated orally with 5 mg kg À1 TCDD or vehicle (day 0) and, 7 days later, colitis was induced by feeding 3% DSS dissolved in drinking water for 7 days (days [7][8][9][10][11][12][13][14]; the mice were killed 3 days later for evaluations (day 17) (Figure 1a). …”

“…13,14 In addition, the activation of AhR induces PGE2 production in certain types of cells, both in vitro and in vivo. 15,16 Therefore, the effects of TCDD on PGE2 expression in the mouse colon were examined to investigate the possible mechanisms underlying the inhibitory effects of TCDD on DSS-induced colitis.…”

Scarless wound healing gel with Binahong (Anredera cordifolia (Ten) Steenis) leaves extract and celecoxib as the active ingredients

“…Celecoxib is suggested to play a role in the inflammation phase (1 st phase) of the wound healing processes [2,8]. Both ursolic acid and celecoxib inhibit inflammation mediator prostaglandins [9][10][11]. As phytosterol, ursolic acid inhibits phospholipase [11] while celecoxib inhibits COX-2 [12,13] in the cascade of prostaglandin synthase [2,12,14,15].…”

Construction and Optimization of Structure-Based Virtual Screening Protocols to Identify Cyclooxygenase-1 Inhibitors Using Open Babel, Spores and Plants

“…Although celecoxib still remains in the market [2], these withdrawals highlight the association of selective COX-2 inhibitors with the cardiovascular side effects. To avoid both the GI toxicities and the cardiovascular side effects of the anti-inflammatory agents, a new strategy involving discovery and development dual COX-1/COX-2 inhibitors instead of highly selective inhibitors either for COX-1 or COX-2 has been proposed [5][6].…”