β-Caryophyllene attenuates dextran sulfate sodium-induced colitis in mice via modulation of gene expression associated mainly with colon inflammation

Toxicology Reports

Jae Young Cho¹  Jung Han Yoon Park²  Hyang Sook Chun³  Hwa Yeon Kim³  Hong Jin Lee³  Sung-Kyu Kim⁴ 

[1] CKD Research Institute, Dongbaekjukjeon-daero 315-20, Yungin, Kyonggi 446-916, Republic of Korea;Department of Food Science and Nutrition, Hallym University, Hallymdaehak-gil 39, Chuncheon, Kangwon 200-702, Republic of Korea;Department of Food Science and Technology, Chung-Ang University, Naeri 72-1, Ansung, Kyonggi 456-756, Republic of Korea;Nutra R&BT Inc., 371-47 Gasan, Geumcheon-gu, Seoul 153-788, Republic of Korea;

关键词: β-Caryophyllene (PubChem CID5281515);    Colitis;    Dextran sulfate sodium;    Gene expression;    Inflammation;   

DOI  :  10.1016/j.toxrep.2015.07.018

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown