The modulation of COX mediated pathways in UC-associated inflammation was observed by protein expressions of various pro-inflammatory cytokines such as TNF-α and enzymes of PG synthesis such as COX-2, PGES, TXAS, and anti-inflammatory PGDS.
To carry out a systematic review and meta-analysis of previous studies examining the association between acetaminophen and NSAIDs including cyclooxygenase (COX-2) inhibitors use, and risk of Crohn's disease (CD) and ulcerative colitis (UC) exacerbation.
Moreover, AGNE suppressed the increased expression of COX-2 and HIF-1α and the increased production of PGE<sub>2</sub> in colon tissue were observed in mice with DSS-induced UC.
In addition, treatment with D‑limonene significantly increased antioxidant, inducible nitric oxide synthase (iNOS) and cyclooxygenase‑2 (COX‑2) protein expression levels in UC rats.
Our study for the first time demonstrated differential expression of the PGE2-related enzymes COX-2 and 15-PGDH in colonic mucosa from UC, CD, and acute DD.
To determine the effect of non-selective cyclooxygenase (COX) inhibitors, selective COX-2 inhibitors and nitric oxide (NO)-releasing aspirin in the healing of ulcerative colitis.
COX-2A-1195G polymorphism was associated with the risk of UC, especially among never-smokers, suggesting that low activity of COX-2 may predispose to UC.
An effect of the COX-2 polymorphism on both CD and UC was shown which is compatible with the presence of a recessive allele in linkage equilibrium with the SNP marker in the COX-2 gene.
The aim of the present study was: 1) to examine the expression of ghrelin and TNF-alpha mRNA in the inflamed colonic mucosa of patients with ulcerative colitis (UC), 2) to analyze the effect of treatment with exogenous ghrelin on the healing of trinitrobenze sulphonic acid (TNBS)-induced colitis in rats, and 3) to assess the effects of ghrelin treatment on mRNA expression for iNOS and protein expression for COX-2 and PPARalpha in intact colonic mucosa and in that with TNBS-induced colitis.
COX-2 expression was absent from normal colon, whereas in Crohn's colitis and ulcerative colitis, COX-2 was observed in apical epithelial cells and in lamina propria mononuclear cells.