Baicalein Inhibits Dextran Sulfate Sodium-induced Mouse Colitis
10.15430/JCP.2019.24.2.129
- Author:
Xiancai ZHONG
1
;
Young Joon SURH
;
Seon Gil DO
;
Eunju SHIN
;
Kyu Suk SHIM
;
Chong Kil LEE
;
Hye Kyung NA
Author Information
1. Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Korea. surh@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Baicalein;
Colitis;
NF-κB;
Cyclooxygenase-2;
Anti-inflammation
- MeSH:
Adenosine Triphosphate;
Animals;
Asian Continental Ancestry Group;
Blotting, Western;
Carcinogenesis;
Colitis;
Colon;
Curcuma;
Curcumin;
Cyclin D1;
Cyclooxygenase 2;
Dextran Sulfate;
Dextrans;
DNA;
Drinking Water;
Herbal Medicine;
Humans;
Inflammatory Bowel Diseases;
Mice;
Nitric Oxide Synthase Type II;
Phosphorylation;
Phosphotransferases;
Plants;
Scutellaria baicalensis
- From:Journal of Cancer Prevention
2019;24(2):129-138
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Baicalein is a bioactive flavone that is originally extracted from the root of Scutellaria baicalensis Georgi. This plant has long served as Chinese herbal medicine in the management of multiple diseases including inflammatory bowel diseases. Although it has been revealed that baicalein inhibits experimental colitis in mice, the molecular mechanisms still remain largely unrecognized. METHODS: The experimental colitis was induced in mice by 3% dextran sulfate sodium (DSS) in drinking water. The mice were given baicalein (10 or 25 mg/kg) by gavage for 7 days before and after DSS administration. Expression of COX-2 and inducible nitric oxide synthase (iNOS) and molecules involved in NF-κB signaling, such as inhibitor of κBα (IκBα), pIκBα, p65, and phospho-p65 was examined by Western blot analysis in the tissue of the mouse colon. Activity of IκB kinase β (IKKβ) was assessed by measuring the relative amount of radioactive γ-phosphate of ATP transferred to the IκBα substrate protein. The expression and phosphorylation of STAT3 and its target gene cyclin D1 were also measured. RESULTS: Baicalein prominently mitigated the severity of DSS-induced colitis in mice. It inhibited the expression of COX-2 and iNOS. Moreover, baicalein attenuated activity and phosphorylation of IKKβ and subsequent degradation of IκBα. Baicalein suppressed the phosphorylation and nuclear translocation of p65, resulting in a reduced DNA binding activity of NF-κB. Baicalein also suppressed the phosphorylation of STAT3 and expression of cyclin D1. Baicalein exhibited the synergistic effect on inhibition of COX-2 induced by DSS with curcumin, an ingredient of turmeric. CONCLUSIONS: Protective effects of baicalein on DSS-induced colitis are associated with suppression of NF-κB and STAT3 signaling pathways, which may contribute to its cancer preventive effects on colon carcinogenesis.
