Journal
TOXICOLOGY REPORTS
Volume 2, Issue -, Pages 1039-1045Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.toxrep.2015.07.018
Keywords
beta-Caryophyllene (PubChem CID5281515); Colitis; Dextran sulfate sodium; Gene expression; Inflammation
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Funding
- National Research Foundation (NRF) [NRF-2013M3A9C4078156]
- Chung-Ang University Excellent Student Scholarship
- National Research Foundation of Korea [2013M3A9C4078156] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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We examined the modulatory activity of beta-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-1 beta, 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-kappa B 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-kappa B activity. (C) 2015 Published by Elsevier Ireland Ltd.
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