Colon inflammation

Colon inflammation 1. AEA levels are elevated in the colon of DNBS-treated mice and in the colon submucosa of TNBS-treated rats, two animal models of inflammatory bowel diseases, and in the biopsies of patients with ulcerative colitis, to control inflammation 1. Inhibitors of degradation (both FAAH and cellular re-uptake)... 

Fretland, D.J., Widomski, D.L., Anglin, C.P., Levin, S. and Gagjnella, T.S. (1990). Colonic inflammation in the rodent induced by phorbol-12-myristate-13-acetate a potential model of inflammatory bowel disease, effect of SC-41930. Gastroenterology 98, A449. 

Keshavarzian, A., Doria, M.I., Sedghi, S., Kanofeky, J.R., Hecht, D., Holmes, E.W., Ibrahim, C., List, T., Urban, G., Gaginella, T. and Fields, J.Z. (1992a). Mitomycin C-induced colitis in rats a new animal model of acute colonic inflammation implicating reactive oxygen metabolites. J. Lab. Clin. Med. 120, 778-791. 

Mechanism of action of mesalamine is unknown, but appears topical rather than systemic. It may diminish colonic inflammation by blocking cyclooxygenase and inhibiting colon prostaglandin production in bowel mucosa. 

Mechanism of Action Asalicylicacidderivativethat isconvertedtomesalamineinthe colon by bacterial action. Blocks prostaglandin production in bowel mucosa. Therapeutic Effect Reduces colonic inflammation in inflammatory bowel disease. Pharmacokinetics Small amount absorbed. Protein binding 99%. Metabolized by bacteria in the colon. Minimal elimination in urine and feces. Half-life 0.9 hr. 

Martin AR, Villegas I, La Casa C, de la Lastra CA. 2004. Resveratrol, a polyphenol found in grapes, suppresses oxidative damage and stimulates apoptosis during early colonic inflammation in rats. Biochem Pharmacol 67 1399-1410. 

Desreumaux, P., Dubuquoy, L., Nutten, S., Peuchmaur, M., Englaro, W., Schoonjans, K., Derijard, B., Desvergne, B., Wahli, W., Chambon, P., Leibowitz, M. D., Colombel, J. F., et al. (2001). Attenuation of colon inflammation through activators of the retinoid X receptor (RXR)/ peroxisome proliferator-activated receptor gamma (PPARgamma) heterodimer. A basis for new... 

Grisham MB, MacDermott RP, Deitch EA (1990) Oxidant defense mechanisms in human colon. Inflammation 14 669-680... 

Almost all antibacterial agents have been observed to cause diarrhea in a variable proportion of patients (114,115). The proportion depends not only on the antibiotic, but also on the clinical setting (in-patient/out-patient), age, race, and the definition of diarrhea. Severe colonic inflammation develops in a variable proportion of cases, and in some cases pseudomembranous colitis occurs (116-121). Since 1977, much evidence has accumulated that the most important causative agent in antibiotic-associated diarrhea is an anaerobic, Gram-positive, toxin-producing bacterium, C. difficile (122-124). 

The causal connection between NSAIDs and large bowel inflammation needs to be confirmed by appropriate epidemiological studies. Many publications have associated NSAID and colonic inflammation (SEDA-10, 77) (SEDA-15, 95), but the differential diagnosis between colonic inflammation arising de novo and exacerbation of underlying inflammatory bowel disease can be difficult, and the role of NSAIDs in aggravating ulcerative colitis or Crohn s disease or other inflammatory bowel disease is controversial (SEDA-10, 76) (SEDA-15, 95). A case-control study showed no association between appendi-cectomy for acute appendicitis and the use of NSAIDs (SEDA-22, 111). 

Massa F, Marsicano G, Hermann H, Cannich A, Monory K, Cravatt BF, Ferri GL, Sibaev A, Storr M, Lutz B (2004) The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 1202-1209... 

Monosubstituted Mn(ii)-based complexes, which catalyze the dismutation of superoxide as shown by stopped-flow kinetic analysis, were tested for antiinflammatory activity in the mouse acetic acid-induced colitis model. As can be seen from Table 3, all of the SOD mimics are anti-inflammatory. Histological analysis of the colonic tissue confirmed these results. Of particular importance is the observation that Mn(ii) complexes that have no SOD activity, specifically the Mn(ii) dichloro complexes of 1,4,7,10,13-pentaazacyclohexadecane and 1,4,7,11,14-pentaazacycloheptadecane, do not protect against the colonic inflammation induced by acetic acid when the compounds are administered in-tracolonically at a dose of 30mgkg These results are consistent with a role for superoxide as a mediator of neutrophil-dependent inflammation. Consistent with this hypothesis is the observation that SC-52608 inhibits neutrophil-dependent inflammation induced by the intradermal administration of leukotriene 64, a neutrophil chemoattractant. ... 

Sulfasalazine is a pro-drug that is not active in its ingested form. It is broken down by colonic bacteria into 5-aminosalicylic acid (5-ASA mesalamine) and sulfapyridine. Some controversy exists regarding which of these two products are responsible for the activity of azulfidine. 5-Aminosalicylic acid, however, is known to have a therapeutic benefit, although it is not clear whether sulfapyridine adds any further benefit. In the colon, the products created by the breakdown of sulfasalazine work as anti-inflammatory agents for treating colon inflammation. The beneficiai effect of sulfasalazine is believed to result from a local effect on the bowel, although there also may be a beneficial systemic immune-suppressant effect. Sulfasalazine was approved in 1950. 

ECM is facilitated by small hyaluronic acid molecules implies a function in host defense, but has not been proven (106). Increased levels of hyaluronic acid were associated with colon inflammation, psoriasis, osteoarthritis, rheumatoid arthritis, and scleroderma (101,107,108), as well as with viral infections (109). Hyaluronic acid is produced by endothelial cells and binds to its receptor, CD44, expressed by activated T and B cells, inducing the attachment of the two cell types (110). This interaction is controlled by the expression of specific hyaluronic acids sub-types or by modifications of CD44 on platelets (111). High molecular weight hyaluronic acid and CD44 are essential for scarless embryonic wound repair (112). 

Kiss J, Lamarque D, Delchier JC et al. Time-dependent actions of nitric oxide synthase inhibition on colonic inflammation induced by trinitrobenzene sulphonic acid in rats. Eur J Pharmacol 1997 336 219-24. 

Derijard, B. Desvergne, W. Wahli, P. Chambon, et al. Attenuation of Colon Inflammation through Activators of the Retinoid X Receptor (RXR)/Peroxisome Proliferator-Activated Receptor y (PPARy) Heterodimer. A Basis for New Therapeutic Strategies,... 

Tardieu, D. Jaeg, J.P. Deloly, A. Carpet, E.D. Cadet, J. Petit, C.R. The COX-2 inhibitor nimesulide suppresses superoxide and 8-hydroxy-deoxyguanosine formation, and stimulates apoptosis in mucosa during early colonic inflammation in rats. Carcinogenesis 2000, 21 (5), 973-976. 

Takeda Y, Nakase H, Namba K, et al. Upregulation of T-bet and tight junction molecules by Bifidobactrium longum improves colonic inflammation of ulcerative colitis. Inflamm Bowel Dis. 2009 15 1617-1618. 

Castagnini C, Luceri C, Toti S, et al. Reduction of colonic inflammation in HLA-B27 transgenic rats by feeding Marie Menard apples, rich in polyphenols. Br J Nutr. 2009 102(11) 1620—1628. 

Sanchez-Fidaigo S, Cardeno A, Villegas I, Xaiero E, de la Lastra CA (2010) Dietary supplementation of resveratroi attenuates chronic colonic inflammation in mice. Eur J Pharmacol 633 78-84... 

K. Azuma, T. Osaki, S. Ifuku, H. Maeda, M. Morimoto, O. Takashima, T. Tsuka, T. Imagawa, Y. Okamoto, H. Saimoto, and S. Minami, Suppressive effects of cellulose nanofibers—made from adlay and seaweed—on colon inflammation in an inflammatory bowel-disease model, Bioact. Carbohydr. Diet. Fibre, 2(1), 65-72,2013. 

Busserolles, J., Paya, M., D Auria, M.V., Gomez-Paloma, L., Alcaraz, M.J., 2005. Protection against 2,4,6-tiinitrobenzenesulphonic acid-induced colonic inflammation in mice by the marine products bolinaquinone and petrosaspongiohde M. Biochem. Pharmacol. 69, 1433-1440. 

Kruidenier, L., van Meeteren, M.E., Kuiper, I., et al. (2003) Attenuated mild colonic inflammation and improved survival from severe DSS-cohhs of transgenic Cu/Zn-SOD mice. Free Rad Biol Med 34, 753-765. 

Martui, R., Cham, R, Miquel, S., et al. (2014) Effects in the use of a genetically engineered strain of Lactococcus lactis delivering in situ II IO as a therapy to treat low-grade colon inflammation. Hum Vaccin Immunother 10, 1611-1621. 

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