Journal
ONCOTARGET
Volume 8, Issue 37, Pages 61385-61392Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.18219
Keywords
genistein; inflammation; barrier; NF-kappa B; mice
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Funding
- National Natural Science Fund from the National Natural Science Foundation of China [81672427]
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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-kappa B signal. In conclusion, genistein alleviated DSS-caused colonic injury, inflammation, and gut dysfunction, which might be associated with the TLR4/NF-kappa B signal.
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