Genistein improves inflammatory response and colonic function through NF-κB signal in DSS-induced colonic injury
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Rui Zhang1, Jian Xu1, Jian Zhao1 and Yuzhe Chen1
1Department of Colorectal Surgery, Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning Province, P. R. China
Yuzhe Chen, email: email@example.com
Keywords: genistein, inflammation, barrier, NF-κB, mice
Received: March 14, 2017 Accepted: April 05, 2017 Published: May 26, 2017
This study aimed to investigate the protective potential of genistein in dextran sulfate sodium (DSS)-induced colonic injury in vitro and in vivo models. The results showed that DSS exposure caused growth suppression, colonic injury, inflammation, and barrier dysfunction in mice. Dietary genistein alleviated DSS-caused colonic injury via reducing colonic weight, rectal bleeding, and diarrhea ratio. Meanwhile, genistein reduced colonic inflammatory response via downregulating cytokines expression and improved colonic permeability and barrier in DSS-challenged mice. In Caco-2 cells, genistein improved cell viability and cellular permeability and inhibited DSS-induced activation of TLR4/NF-κB signal. In conclusion, genistein alleviated DSS-caused colonic injury, inflammation, and gut dysfunction, which might be associated with the TLR4/NF-κB signal.
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