Acetyl-11-keto-β-boswellic Acid Confers Protection in DSS-Induced Colitis via the JNK-p38 MAPK and NF-κB Signaling Pathways.

Abstract

The present study aims to explore the effect and mechanismofacetyl-11-keto-β-boswellic acid (AKBA) on inflammatory bowel disease (IBD). The IBD-mouse model is established by replacing normal water intake with 2.5% dextran sulfate sodium salt (DSS) aqueous solution, and 50mg kg-1 of AKBA treatment is administered. The experimental mice are randomly divided into four groups, including control, AKBA , DSS, and DSS + AKBA groups. AKBA therapy conspicuously ameliorates the adverse symptoms caused by DSS in mice and inhibits the reduction of colon length and the rise of disease activity index score. Hematoxylin-eosin staining results suggest that AKBA strikingly improves the pathological conditions of the colon and small intestine tissues in IBD mice. AKBA prominently inhibits the DSS-induced increase of proinflammatory factor contents and the upregulation of the c-Jun N-terminal kinase (JNK)-p38/mitogen-activated protein kinase (MAPK) and Nuclear factor kappa B (NF-κB) pathways' protein levels in the colon tissues of IBD mice. AKBA alleviates DSS-induced colonic inflammatory injury in IBD mice by repressing the activation of the JNK-p38/MAPK and NF-κB pathways.