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DOI: 10.1055/s-0030-1250462
© Georg Thieme Verlag KG Stuttgart · New York
Polydatin Ameliorates DSS-Induced Colitis in Mice through Inhibition of Nuclear Factor-kappaB Activation
Publication History
received February 2, 2010
revised August 13, 2010
accepted Sept. 28, 2010
Publication Date:
26 October 2010 (online)
![](https://www.thieme-connect.de/media/plantamedica/201105/lookinside/thumbnails/10.1055-s-0030-1250462-1.jpg)
Abstract
Nuclear factor-κB (NF-κB) plays a pivotal role in the regulation of immune and inflammatory responses. The real-time expression level of NF-κB reflects the development of ulcerative colitis (UC). Polydatin has vast pharmacological activities, including inhibiting the production of inflammatory mediators, inducing the production of antioxidants, regulating immune function, etc. The purpose of this study was to investigate the potential inhibitory effects of polydatin on NF-κB pathway activation in a mouse UC model. The results showed that polydatin treatment downregulated NF-κB p65 activity and expression, blocked the expression of TNF-α, IL-6 and IL-1β at both mRNA and protein levels, decreased myeloperoxidase (MPO) activity, and alleviated inflammatory damage of colitis in mice with UC (p < 0.05), suggesting that the anti-inflammation effects of polydatin can be attributed, at least partially, to the blocking of the NF-κB pathway.
Key words
nuclear factor‐κB - polydatin - resveratrol - ulcerative colitis
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Prof. Dr. Li-Sheng Wang
Department of Gastroenterology
Shenzhen Municipal People's Hospital
Jinan University of Medical Sciences
1017 East Gate Road
Shenzhen 518020
Guangdong Province
People's Republic of China
Phone: +86 7 55 25 53 30 18
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