Colitis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Meanwhile, APE supplementation decreased dextran sulphate sodium (DSS)-induced colitis in mice, ameliorating epithelial barrier disruption, suppressing the proliferation and infiltration of immune cells, modulating the secretion of nitric oxide (NO) and prostaglandin E2 (PGE2), decreasing the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as regulating oxidative stress in vivo.
|
31204754 |
2019 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
On DSS administration to Nrf2<sup>-/-</sup> mice, colitis was significantly aggravated (p < 0.01), in which the expressions of COX-2 as well as expressions of HO-1 and γ-GCS were significantly increased (p < 0.01).
|
30683827 |
2018 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Mice receiving rectal insulin enemas exhibited lower colitis endoscopic scores and reduced cyclooxygenase 2 mRNA expression, and developed significantly fewer and smaller tumours compared with the control group receiving phosphate-buffered saline only.
|
30137286 |
2018 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Further investigation showed a decreased expression of COX-2 and iNOS in the colonic tissue of colitis mice, two important mediators of intestinal inflammation, but there was no inhibition of the gelatinase MMP-9 and MMP-2 activities.
|
28494341 |
2017 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In addition, AG inhibited the production of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, and the protein expression of COX-2 and iNOS in mice with DSS-induced colitis.
|
28695925 |
2017 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
IBD98-M treatment also reduced myeloperoxidase activity and the expression levels of cyclooxygenase 2 and tumor necrosis factor-αin the colitis tissue.
|
28556814 |
2017 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In addition, RA resulted in the reduction of the inflammatory-related cytokines, such as IL-6, IL-1β, and IL-22, and protein levels of COX-2 and iNOS in mice with DSS-induced colitis.
|
28383063 |
2017 |
Colitis
|
0.600 |
Biomarker
|
disease |
BEFREE |
To our knowledge, this is the first study to demonstrate that Gent treatment can exert anti-inflammatory effects on experimental acute colitis through attenuating the expression levels of TNF-α, IL-1β, IL-6, iNOS and COX-2, and it may present the therapeutic potential in the treatment of colitis.
|
27394986 |
2016 |
Colitis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Rats with 2,4,6 trinitrobenzenesulfon-ic acid (TNBS)-induced colitis received intragastric (ig) treatment with vehicle, aspirin (ASA) (a non-selective COX inhibitor), celecoxib (a selective COX-2 inhibitor) or NO-releasing ASA for a period of ten days.
|
22039321 |
2011 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Since COX-2 isoform is overexpressed in colic inflammatory states, we examined the inhibitory effect of COX-2-inhibitors on P-gp expression and function under COX-2 stimulated conditions mediated by trinitrobenzene sulfonic acid (TNBS) in vitro, in Caco-2 cells, and in TNBS-induced colitis in mice.
|
20361960 |
2010 |
Colitis
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In rats the exogenous ghrelin administered daily at a dose of 20 microg/kg i.p. significantly accelerated the healing of TNBS colitis and this effect was accompanied by an increase in mRNA expression for iNOS and protein expression for COX-2 in the colonic mucosa.
|
19617644 |
2009 |
Colitis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Because TNF-alpha and COX-2 are increased in patients with inflammatory bowel disease (IBD), we investigated the role of SK1 in a murine model of colitis.
|
18815359 |
2009 |
Colitis
|
0.600 |
Therapeutic
|
disease |
RGD |
Glutamine inhibits over-expression of pro-inflammatory genes and down-regulates the nuclear factor kappaB pathway in an experimental model of colitis in the rat.
|
17543437 |
2007 |
Colitis
|
0.600 |
Biomarker
|
disease |
CTD_human |
TNBS-induced colitis was associated with enhanced COX-2 expression in the gut and increased circulating concentrations of PGE2 metabolite (PGEM).
|
11820457 |
2001 |
Colitis
|
0.600 |
Biomarker
|
disease |
BEFREE |
Thus, COX-2-derived PG presumably plays a role in the repair process of gastritis, ulcers, and colitis.
|
9773924 |
1998 |