Prdx6-induced inhibition of ferroptosis in epithelial cells contributes to liquiritin-exerted alleviation of colitis

甘草苷 结肠炎 铁蛋白 化学 炎症 药理学 生物化学 免疫学 医学 色谱法 高效液相色谱法
作者
Jinming Liu,Liqun Sun,Dapeng Chen,Xiaokui Huo,Xiangge Tian,Juan Li,Min Liu,Zhenlong Yu,Baojing Zhang,Yuewen Yang,Yang Qiu,Yuejian Liu,Huishu Guo,Changjiang Zhou,Xiaochi Ma,Yongjian Xiong
出处
期刊:Food & Function [The Royal Society of Chemistry]
卷期号:13 (18): 9470-9480 被引量:31
标识
DOI:10.1039/d2fo00945e
摘要

Inhibition of ferroptosis in intestinal epithelial cells ameliorates clinical symptoms and improves endoscopic presentations in inflammatory bowel disease (IBD). Licorice is used worldwide in food and medicine fields. Liquiritin, a flavonoid component in licorice, is an effective substance used as an anti-inflammatory, antioxidant food that has been shown to improve chemically induced colitis. Herein we evaluated the therapeutic effects of liquiritin on colitis and determined whether liquiritin could affect colitis by modulating ferroptosis in epithelial cells. A colitis model was induced in mice by oral administration with 2.5% DSS dissolved in drinking water. The results showed that liquiritin significantly alleviated symptoms, suppressed intestinal inflammation and restored the epithelial barrier function in the colitis mouse model. Liquiritin supplementation upregulated colonic ferritin expression, increased the storage of cellular iron, reduced the cellular iron level and further inhibited ferroptosis in epithelial cells from the colitis model. Pharmacological stimulation of ferroptosis largely blocked liquiritin-induced alleviation of colitis. Peroxiredoxin-6 (Prdx6) expression was significantly decreased in the DSS group, which was reversed by liquiritin treatment. Genetic or pharmacological silencing of Prdx6 largely reversed liquiritin-induced modulation of the ferritin/iron level and ferroptosis in epithelial cells. Molecular docking results showed that liquiritin could bind to Prdx6 through the hydrogen bond interaction with amino acid residues Thr208, Val206 and Pro203. In conclusion, liquiritin treatment largely alleviated DSS induced colitis by inhibiting ferroptosis in epithelial cells. Liquiritin negatively regulated ferroptosis in epithelial cells in colitis by activating Prdx6, increasing the expression of ferritin and subsequently reducing the cellular iron level.
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