Figure 2. 2-Cl-IB-MECA administration reduced inflammation and tissue injury, inhibited MPO activity, and decreased TNF-a and IL-1β expression in DSS-induced murine colitis.

(A) 2-Cl-IBMECA administration reduced H&E histopathology in murine DSS colitis. In normal mice, there was no active inflammation, crypt or surface epithelial damage, or ulceration. In mice treated with 5% DSS with or without DMSO, transmural inflammation, crypt damage, and ulceration were observed. In 5% DSS with 2-Cl-IB-MECA, focal active inflammation without crypt or surface epithelial damage or ulceration was observed. (B) 2-Cl-IB-MECA administration protects mice from gut inflammation and tissue injury. Aggregate histopathological scoring of inflammation, ulceration, and crypt damage indicates protection. A Mann–Whitney nonparametric U-test was used. (C) 2-Cl-IB-MECA inhibits MPO activity after DSS induction of colitis. MPO elevation in DSS-induced colitis is reduced by 2-Cl-IB-MECA administration. TNF-a (D) and IL-1β (E) mRNA were expressed at relatively low levels in the normal group. Induction of colitis with 5% DSS resulted in an increase in TNF-a and IL-1β mRNA expression. However, 2-Cl-IB-MECA significantly reduced DSS-induced TNF-a and IL-1β mRNA expression in colitis mice. No significant difference was observed between vehicle-treated mice with DSS colitis and mice with DSS colitis alone. Data are presented as mean ± SD of three independent experiments (*P < 0.01 compared with the normal group; #P < 0.05 compared with the DSS group).