Effects of topical 5-aminosalicylic acid and prednisolone on prostaglandin E2 and leukotriene B4 levels determined by equilibrium in vivo dialysis of rectum in relapsing ulcerative colitis

Lauritsen, K; Laursen, L. C.; Bukhave, Klaus; Rask-Madsen, J

doi:10.1016/0016-5085(86)90684-0

Cited by 247 publications

(89 citation statements)

References 34 publications

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“…Table 3 summarizes the studies on treatment of radiation damage to various organs of the digestive system with anti-inflammatory drugs. The results obtained by using the prodrug sulphasalazine which yields in the large bowel the active principle, 5-amino-salicylic acid, have been enclosed because its multitudinous mechanisms of therapeutic action in inflammatory bowel disease include inhibition of eicosanoid synthesis (245)(246)(247). Broader issues of radiation enterocolitis in man are addressed by a recent monograph (248).…”

Section: Anti-inflammatory Drugs Modify the Development Of Radiation mentioning

confidence: 99%

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

Michałowski

1994

Acta Oncologica

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Section: Anti-inflammatory Drugs Modify the Development Of Radiation mentioning

confidence: 99%

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

Michałowski

1994

Acta Oncologica

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“…Inflammatory bowel disease also seems to be associated with perturbations in lipid metabolism. In fact, increased levels of prostaglandin E 2 and leukotriene B 4 are found in intestinal mucosa from patients with inflammatory bowel disease and have been suggested to play an important role in its pathogenesis (Sharon & Stenson 1984, Lauritsen et al 1986. Furthermore, changing the quality of dietary fat has been shown to beneficially influence inflammatory bowel disorders (Lee & Austen 1985, Stenson et al 1992, Belluzi et al 1996.…”

Section: Introductionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor gamma is induced during differentiation of colon epithelium cells

Lefebvre¹,

Paulweber²,

Fajas³

et al. 1999

Journal of Endocrinology

149

104

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Peroxisome proliferator-activated receptor (PPAR ), a fatty acid-activated nuclear receptor, is implicated in adipocyte differentiation and insulin sensitisation. In view of the association of dietary fat intake and bowel disease, the expression of PPAR in rodent and human intestine was studied. Expression of PPAR mRNA was examined by Northern blot hybridisation, RNase protection, and/or competitive RT-PCR assays, whereas PPAR protein levels were evaluated by immunoblotting and immunohistochemistry. PPAR mRNA and protein were abundantly expressed in colon relative to the small intestine both in rodents and in man. Interestingly, expression of PPAR was primarily localised in the more differentiated epithelial cells in the colon. The level of expression of PPAR in colon was similar to the levels seen in adipose tissue. Expression of PPAR increased from proximal to distal segments of the colon in man. In Caco-2 and HT-29 human adenocarcinoma cells, PPAR expression increased upon differentiation, consistent with PPAR being associated with a differentiated epithelial phenotype. High-level expression of PPAR was observed in the colon, but not in the small intestine, suggesting a potential role of this nuclear receptor in the colon.

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“…Through generation of PGs, COX-2 regulates diverse biological responses, including cell survival (28,68,71), proliferation (58), and migration (10), that promote homeostasis of the colon epithelial monolayer. COX-2 is thought to be important in IBD, because COX-2 protein expression and PG levels are elevated in the GI tract of IBD patients (32,59,62). However, whether COX-2 is pathogenic or cytoprotective in IBD is unclear.…”

mentioning

confidence: 99%

TNF transactivation of EGFR stimulates cytoprotective COX-2 expression in gastrointestinal epithelial cells

Hobbs¹,

Goettel

Liang³

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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TNF and epidermal growth factor (EGF) are well-known stimuli of cyclooxygenase (COX)-2 expression, and TNF stimulates transactivation of EGF receptor (EGFR) signaling to promote survival in colon epithelial cells. We hypothesized that COX-2 induction and cell survival signaling downstream of TNF are mediated by EGFR transactivation. TNF treatment was more cytotoxic to COX-2−/−mouse colon epithelial (MCE) cells than wild-type (WT) young adult mouse colon (YAMC) epithelial cells or COX-1−/−cells. TNF also induced COX-2 protein and mRNA expression in YAMC cells, but blockade of EGFR kinase activity or expression inhibited COX-2 upregulation. TNF-induced COX-2 expression was reduced and absent in EGFR−/−and TNF receptor-1 (TNFR1) knockout MCE cells, respectively, but was restored upon expression of the WT receptors. Inhibition of mediators of EGFR transactivation, Src family kinases and p38 MAPK, blocked TNF-induced COX-2 protein and mRNA expression. Finally, TNF injection increased COX-2 expression in colon epithelium of WT, but not kinase-defective EGFRwa2and EGFRwa5, mice. These data indicate that TNFR1-dependent transactivation of EGFR through a p38- and/or an Src-dependent mechanism stimulates COX-2 expression to promote cell survival. This highlights an EGFR-dependent cell signaling pathway and response that may be significant in colitis-associated carcinoma.

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Effects of topical 5-aminosalicylic acid and prednisolone on prostaglandin E2 and leukotriene B4 levels determined by equilibrium in vivo dialysis of rectum in relapsing ulcerative colitis

Cited by 247 publications

References 34 publications

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

On Radiation Damage to Normal Tissues and its Treatment: II. Anti-inflammatory drugs

Peroxisome proliferator-activated receptor gamma is induced during differentiation of colon epithelium cells

TNF transactivation of EGFR stimulates cytoprotective COX-2 expression in gastrointestinal epithelial cells

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