Acertannin prevented dextran sulfate sodium-induced colitis by inhibiting the colonic expression of IL-23 and TNF-alfa in C57BL.6J mice
Acertannin prevented dextran sulfate sodium-induced colitis by inhibiting the colonic expression of IL-23 and TNF-alfa in C57BL.6J mice
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醋单宁通过抑制 C57BL.6J 小鼠结肠中 IL-23 和 TNF-α 的表达来预防葡聚糖硫酸钠诱导的结肠炎
DOI:
10.1055/a-2037-2995
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发表时间:
2023
期刊:
影响因子:
2.7
通讯作者:
T. Okuda
中科院分区:
文献类型:
--
作者:
Y. Kimura;M. Taniguchi;T. Okuda
The present study investigates the effects of acertannin on colitis induced by dextran sulfate sodium (DSS) and changes in the colonic levels of the cytokines interleukin (IL)-1β, IL-6, IL-10, IL-23, tumor necrosis factor (TNF)-α, the chemokine monocyte chemoattractant protein (MCP)-1, and vascular endothelial growth factor (VEGF).We examine the following: inflammatory colitis was induced in mice by 2% DSS drinking water givenad libitumfor 7 days. Red blood cell, platelets, and leukocyte counts and hematocrit (Ht), hemoglobin (Hb), and colonic cytokine and chemokine levels were measured. The disease activity index (DAI) was lower in DSS-treated mice orally administered acertannin (30 and 100 mg/kg) than in DSS-treated mice. Acertannin (100 mg/kg) inhibited reductions in the red blood cell count and Hb and Ht levels in DSS-treated mice. Acertannin prevented DDS-induced mucosal membrane ulceration of the colon and significantly inhibited the increased colonic levels of IL-23 and TNF-α. Our findings suggest that acertannin has potential as a treatment for inflammatory bowel disease (IBD).