Β-Caryophyllene attenuates dextran sulfate sodium-induced colitis in mice via modulation of gene expression associated mainly with colon inflammation. (2015)

• Record Type: Journal Article
• Authors: Cho, Jae Young; Kim, Hwa Yeon; Kim, Sung-Kyu; Park, Jung Han Yoon; Lee, Hong Jin; Chun, Hyang Sook
• Is Part Of: Toxicology reports. Volume 2(2015)
• Page Start: 1039
• Page End: 1045
• Publication Date: 2015
• Subjects: CA β-caryophyllene -- CD crohn disease -- Cebpb CCAAT/enhancer-binding protein &beta -- DSS dextran sulfate sodium -- Hp haptoglobin -- IBD inflammatory bowel disease -- IκB inhibitor κB -- IL interleukin -- MPO myeloperoxidase -- NF-κB nuclear factor-kappa B -- S100a8 S100 calcium binding protein a8 -- Saa3 serum amyloid A3 -- SAL sulfasalazine -- TNF-α tumor necrosis factor-α -- UC ulcerative colitis; β-Caryophyllene (PubChem CID5281515) -- Colitis -- Dextran sulfate sodium -- Gene expression -- Inflammation; Toxicology -- Periodicals; Clinical toxicology -- Periodicals; Drug-Related Side Effects and Adverse Reactions; Hazardous Substances; Poisoning; Toxicology; Electronic journals; Periodicals; Periodicals; 571.9505
• DOI: 10.1016/j.toxrep.2015.07.018
• Languages: English
• ISSNs: 2214-7500

Abstract

Abstract: We examined the modulatory activity of β-caryophyllene (CA) and gene expression in colitic colon tissues in a dextran sulfate sodium (DSS)-induced colitis model. Experimental colitis was induced by exposing male BALB/c mice to 5% DSS in drinking water for 7 days. CA (30 or 300 mg/kg) was administered orally once a day together with DSS. CA administration attenuated the increases in the disease activity index, colon weight/length ratio, inflammation score, and myeloperoxidase activity in DSS-treated mice. Microarray analysis showed that CA administration regulated the expression in colon tissue of inflammation-related genes including those for cytokines and chemokines (Ccl2, Ccl7, Ccl11, Ifitm3, IL-1β, IL-28, Tnfrsf1b, Tnfrsf12a); acute-phase proteins (S100a8, Saa3, Hp); adhesion molecules (Cd14, Cd55, Cd68, Mmp3, Mmp10, Sema6b, Sema7a, Anax13); and signal regulatory proteins induced by DSS. CA significantly suppressed NF-κB activity, which mediates the expression of a different set of genes. These results suggest that CA attenuates DSS-induced colitis, possibly by modulating the expression of genes associated mainly with colon inflammation through inhibition of DSS-induced NF-κB activity.