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人体乳外基因组通过抑制人类肠道上皮细胞中REDD1表达诱导ZO-1表达

Takeshi Chiba^1,2, Tomoji Maeda³

¹Faculty of Pharmaceutical Sciences, Hokkaido University of Science.

Biological & pharmaceutical bulletin

|July 2, 2023

概括

人类乳外体 (HME) 通过增加zonula occludens-1 (ZO-1) 和降低REDD1.1来增强肠道屏障功能. 这表明HME可能会保护婴儿免受诸如死性肠炎等疾病的影响.

科学领域:

细胞生物学细胞生物学
胃肠病学胃肠病学
新生儿科学新生儿科学

背景情况:

人类乳外体 (HME) 已知可以改善肠道屏障功能,并减少婴儿的炎症.
死性肠炎 (NEC) 是婴儿的一种严重疾病,通常与肠道屏障功能受损有关.

研究的目的:

研究HME增强肠道屏障功能的细胞内机制.
具体来说,是为了阐明HME诱导的 zonula occludens-1 (ZO-1) 表达在Caco-2细胞中的作用.

主要方法:

Caco-2人类肠道上皮细胞被HME治疗了72小时.
测量了体间电阻 (TEER).
在发育和DNA损伤反应1 (REDD1) 中调节的ZO-1的水平,以及拉巴胺素的机械性标 (mTOR) 通过西式涂抹和RT-PCR进行了评估.
细胞还被化 (CoCl2) 处理,以诱导REDD1.

主要成果:

HME治疗显著增加了TEER和ZO-1蛋白水平.
HME治疗显著降低了REDD1.1的mRNA和蛋白质水平.
HME治疗增加了酸化mTOR (p-mTOR) 和p-mTOR/mTOR比率.
与HME和CoCl2同时治疗逆转了CoCl2引起的ZO-1下降和REDD1.1增加.

结论:

HME通过上调调节ZO-1和下调调节REDD1.1,增强肠道屏障功能.
观察到的p-mTOR的增加表明mTOR信号在HME介导的效应中发挥了作用.
这些发现强调了HME在保护婴儿肠道和预防NEC等疾病方面的潜在治疗作用.

关键词:

母乳是母乳中的一种.外基因组是外基因组中的一个.在发育和DNA损伤反应1中受到调节.紧密的交叉路口紧密的连接区域封闭-1的区域.

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