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 mechanism of acetyl‐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 50 mg 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.