Comparative Effects of Curcumin and Tetrahydrocurcumin on Dextran Sulfate Sodium-induced Colitis and Inflammatory Signaling in Mice
10.15430/JCP.2018.23.1.18
- Author:
Joon yeop YANG
1
;
Xiancai ZHONG
;
Su Jung KIM
;
Do Hee KIM
;
Hyun Soo KIM
;
Jeong Sang LEE
;
Hye Won YUM
;
Jeewoo LEE
;
Hye Kyung NA
;
Young Joon SURH
Author Information
1. Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul, Korea. surh@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Curcumin;
Dextran sulfate sodium-induced colitis;
NF-κB;
STAT3;
Tetrahydrocurcumin
- MeSH:
Animals;
Body Weight;
Carcinogenesis;
Colitis;
Colon;
Curcuma;
Curcumin;
Dextran Sulfate;
Dextrans;
Inflammatory Bowel Diseases;
Medicine, Traditional;
Mice;
Nitric Oxide Synthase Type II
- From:Journal of Cancer Prevention
2018;23(1):18-24
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Curcumin, a yellow ingredient of turmeric (Curcuma longa Linn, Zingiberaceae), has long been used in traditional folk medicine in the management of inflammatory disorders. Although curcumin has been reported to inhibit experimentally-induced colitis and carcinogenesis, the underlying molecular mechanisms remain largely unresolved. METHODS: Murine colitis was induced by dextran sulfate sodium (DSS) which mimics inflammatory bowel disease. Curcumin or tetrahydrocurcumin was given orally (0.1 or 0.25 mmol/kg body weight daily) for 7 days before and together with DSS administration (3% in tap water). Collected colon tissue was used for histologic and biochemical analyses. RESULTS: Administration of curcumin significantly attenuated the severity of DSS-induced colitis and the activation of NF-κB and STAT3 as well as expression of COX-2 and inducible nitric oxide synthase. In contrast to curcumin, its non-electrophilic analogue, tetrahydrocurcumin has much weaker inhibitory effects. CONCLUSIONS: Intragastric administration of curcumin inhibited the experimentally induced murine colitis, which was associated with inhibition of pro-inflammatory signaling mediated by NF-κB and STAT3.
