Pharmacological and biochemical characterization of bradykinin B2 receptors in the mouse colon: Influence of the TNBS-induced colitis

Kallikrein – Kinin System and Coagulation System in Inflammatory Bowel Diseases

“…In this model a specific bradykinin BR2 antagonist (HOE -140) attenuated arthritis but exhibited only minimal preventive effect on enterocolitis suggesting that kinin stimulation via B2R was a more important in arthritis than of enterocolitis (Stadnicki et al, 1999). In dextran sulfate (DDS) -induced colitis model in mice a selective B2R antagonist suppressed shortening of the large intestine (Arai et al, 1999), which was in agreement with future results indicated that intestinal contraction was regulated by B2R (Hara et al, 2007), however demonstrated only limited effect in intestinal inflammatory lesions. Later in human studies we demonstrated the increase in the ratio of B1R to B2R gene expression in relation to the degree of intestinal inflammation, and visualized both B1R and B2R in normal as well as inflammatory human colon and ileum (Stadnicki et al, 2005).…”

The role of the complement and contact systems in the dextran sulfate sodium-induced colitis model: the effect of C1 inhibitor in inflammatory bowel disease

“…In addition, bradykinin can stimulate macrophage secretion of interleukin-1 and tumor necrosis factor, which play a key role in CD (39). Previous studies have shown that Bk 2 R is also upregulated in the murine model, but the therapeutic place of Bk 2 R antagonists has not been addressed (16). In this study, however, we found that Bk 2 R Ϫ/Ϫ mice exposed to DSS were not protected, with similar mucosal damage to the WT colitis mice.…”

Maresin 1, a Proresolving Lipid Mediator Derived from Omega-3 Polyunsaturated Fatty Acids, Exerts Protective Actions in Murine Models of Colitis

“…It has been well established that a single intracolonic administration of TNBS results 72 h later in formation of colonic granulomas associated with infiltration of inflammatory cells in all layers, strong thickening of the intestinal wall, hyperplasia of the epithelium, and ulceration (27,51). Thus, to evaluate the possible anti-inflammatory effect of MaR1 in another model of colitis, we investigated its effect against TNBS-induced gut inflammation.…”