Mesalamine blocks tumor necrosis factor growth inhibition and nuclear factor κB activation in mouse colonocytes

Glucagon-Like Peptide-2 and Common Therapeutics in a Murine Model of Ulcerative Colitis

“…Although such studies have also suggested a potential therapeutic role for growth factors in the treatment of UC, the possibility of interactions between intestinal growth factors and the currently utilized anti-inflammatory agents has not been widely explored. Nonetheless, negative interactions have been previously demonstrated for tumor necrosis factor and the aminosalicylates (Kaiser et al, 1999), as well as for EGF and the corticosteroids (Ménard et al, 1988). In the present study, we have shown, for the first time, that the effects of GLP-2 to reduce mortality, body weight loss, and colonic damage in murine DSS-colitis are not prevented by concomitant ASA treatment, but the beneficial effects of GLP-2 on both survival and CDS are completely abrogated by coadministration of CS.…”

“…The mechanism of action of these agents has not been fully delineated, but likely includes alterations in arachidonic acid metabolism, cytokine release, and/or the pro-inflammatory nuclear factor-B (NF-B) signaling pathway (Nikolaus et al, 2000). However, previous studies have shown that the growth-inhibitory effects of tumor necrosis factor on mouse colonocytes are prevented by aminosalicylates (Kaiser et al, 1999), whereas EGF treatment blocks the effects of glucocorticoids on DNA synthesis in the human fetal intestine (Ménard et al, 1988). Nonetheless, similar studies have not been conducted with GLP-2 and either the aminosalicylates or corticosteroids.…”

Molecular basis of the potential of mesalazine to prevent colorectal cancer

“…Indeed, it is well known that mesalazine can modulate various inflammatory pathways (e.g. production of inflammatory cytokines, activity of inducible nitric oxide synthase, activation of nuclear factor-κB) that are relevant to CRC initiation and progression [13][14][15][16] . There is also evidence that mesalazine inhibits the formation of reactive oxygen species (ROS) from polymorphonuclear leukocytes [17] , which leads to a decrease or complete inhibition of DNA damage, a phenomenon that has been involved in colon carcinogenesis.…”

Progress in understanding the mechanisms of action of 5-aminosalicylic acid

“…Therefore, sulfasalazine has been shown to be a potent inhibitor of NF-B activation, able to suppress NF-B dependent transcription, and able to prevent nuclear translocation of NF-B due to inhibition of IB␣ phosphorylation and subsequent degradation (32). 5-ASA was also demonstrated to inhibit TNF-␣ stimulated nuclear translocation of NF-B and IB␣ degradation (33). Therefore, 5-ASA has been demonstrated to inhibit TNF-␣ stimulated NF-B activation, NF-B nuclear translocation, and degradation of IB␣ (33).…”

“…5-ASA was also demonstrated to inhibit TNF-␣ stimulated nuclear translocation of NF-B and IB␣ degradation (33). Therefore, 5-ASA has been demonstrated to inhibit TNF-␣ stimulated NF-B activation, NF-B nuclear translocation, and degradation of IB␣ (33).…”