Methionine and Its Hydroxyl Analogues Improve Stem Cell Activity To Eliminate Deoxynivalenol-Induced Intestinal Injury by Reactivating Wnt/β-Catenin Signaling
Methionine and Its Hydroxyl Analogues Improve Stem Cell Activity To Eliminate Deoxynivalenol-Induced Intestinal Injury by Reactivating Wnt/β-Catenin Signaling
复制标题
蛋氨酸及其羟基类似物通过重新激活 Wnt/β-连环蛋白信号传导改善干细胞活性，消除脱氧雪腐镰刀菌烯醇诱导的肠损伤
DOI：
10.1021/acs.jafc.9b04442
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发表时间：
2019
影响因子：
6.1
通讯作者：
Xiu-qi Wang
中科院分区：
文献类型：
--
作者：
Jia-yi Zhou;Zhe Wang;Sai-wu Zhang;Hua-lin Lin;Chun-qi Gao;Jiang-chao Zhao;Chengbo Yang;Xiu-qi Wang
The intestinal epithelium is derived from intestinal stem cells (ISCs) and has direct contact with nutrients and toxins. However, whether methionine (Met) or a methionine hydroxyl analogue (2-hydroxy-4-(methylthio)butanoic acid (HMB)) can alleviate deoxynivalenol (DON)-induced intestinal injury remains unknown. Mice were treated orally with Met or HMB on days 1–11 and with DON on days 4–8. On day 12, the mice were sacrificed, and the jejunum was collected for crypt isolation and culture. Mouse enteroids were treated with DON and Met or HMB ex vivo. The results showed that Met and HMB increased the average daily feed intake and average daily gain of the mice. Met and HMB also improved the jejunal structure and barrier integrity and promoted ISC expansion, as indicated by the increased enteroid formation efficiency and area, under DON-induced injury conditions. In addition, DON-induced decreases in ISC activity were rescued Wnt/β-catenin signaling reactivation by Met or HMB in vivo and ex vivo. Collectively, our findings reveal that Met and HMB alleviated DON-induced intestinal injury by improving ISC expansion and reactivating Wnt/β-catenin signaling. Our study thus provides a nutritional intervention for intestinal diseases involving Wnt/β-catenin signaling.
