Peptide Hp(2-20) accelerates healing of TNBS-induced colitis in the rat

摘要: Background and aims Hp(2-20), a Helicobacter pylori-derived peptide interacting with N-formyl receptors (FPRs), accelerates the healing of gastric injury in rats. Whether Hp(2-20) affects recovery inflamed colonic mucosa is unknown. We evaluated whether accelerated 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis explored mechanism(s) underlying any such effect. Methods Fifteen rats underwent rectal administration 250-500 µg/kg/day, or its control Hp1 for 10 days, following induction TNBS. Macroscopic histological damage was quantified using predetermined scores. FPR1, COX-2, TNF-α, TGF-β, HB-EGF tissue transglutaminase (t-TG) messenger RNA (mRNA) expression determined by quantitative polymerase chain reaction; TNF-α COX-2 protein levels Western blotting. Results (1) TNBS-induced compared to controls consistently FPRs mucosa; (2) TNBS upregulated mRNA mucosal t-TG (3) this, exception HB-EGF, significantly counteracted Hp(2-20). Conclusions an FPR agonist, rat. This effect associated significant reduction t-TG. postulate that FPR-dependent pathways may be involved repair mucosa.