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膳食 PlsEtn 可改善 DMH 诱导的结肠癌发生小鼠结肠黏膜炎症应激和 ACF:乙烯基醚键的保护作用。

Dietary PlsEtn Ameliorates Colon Mucosa Inflammatory Stress and ACF in DMH-Induced Colon Carcinogenesis Mice: Protective Role of Vinyl Ether Linkage.

机构信息

Department of Life and Food Sciences, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, 080-8555, Japan.

Food and Biodynamic Chemistry Laboratory, Graduate School of Agricultural Science, Tohoku University, Sendai, 980-0845, Japan.

出版信息

Lipids. 2021 Mar;56(2):167-180. doi: 10.1002/lipd.12283. Epub 2020 Sep 29.

Abstract

Ethanolamine plasmalogen (PlsEtn), a sub-class of ethanolamine glycerophospholipids (EtnGpl), is a universal phospholipid in mammalian membranes. Several researchers are interested in the relationship between colon carcinogenesis and colon PlsEtn levels. Here, we evaluated the functional role of dietary purified EtnGpl from the ascidian muscle (87.3 mol% PlsEtn in EtnGpl) and porcine liver (7.2 mol% PlsEtn in EtnGpl) in 1,2-dimethylhydrazine (DMH)-induced aberrant crypt foci (ACF) in vivo, and elucidated the possible underlying mechanisms behind it. Dietary EtnGpl-suppressed DMH-induced aberrant crypt with one foci (AC1) and total ACF formation (P < 0.05). ACF suppression by dietary ascidian muscle EtnGpl was higher compared with dietary porcine liver EtnGpl. Additionally, dietary EtnGpl decreased DMH-induced oxidative damage, overproduction of TNF-α, and expression of apoptosis-related proteins in the colon mucosa. The effect of dietary ascidian muscle EtnGpl showed superiority compared with dietary porcine liver EtnGpl. Our results demonstrate the mechanisms by which dietary PlsEtn suppress ACF formation and apoptosis. Dietary PlsEtn attained this suppression by reducing colon inflammation and oxidative stress hence a reduction in DMH-induced intestinal impairment. These findings provide new insights about the functional role of dietary PlsEtn during colon carcinogenesis.

摘要

乙醇胺-plasmalogen(PlsEtn),是乙醇胺甘油磷脂(EtnGpl)的一个亚类,是哺乳动物膜中的一种普遍磷脂。一些研究人员对结肠癌发生与结肠 PlsEtn 水平之间的关系感兴趣。在这里,我们评估了来自海鞘肌肉(EtnGpl 中 PlsEtn 占 87.3 mol%)和猪肝脏(EtnGpl 中 PlsEtn 占 7.2 mol%)的饮食纯化乙醇胺甘油磷脂在 1,2-二甲基肼(DMH)诱导的体内异常隐窝病灶(ACF)中的功能作用,并阐明了其背后可能的潜在机制。饮食 EtnGpl 抑制了 DMH 诱导的一个隐窝异常(AC1)和总 ACF 形成(P < 0.05)。饮食海鞘肌肉 EtnGpl 对 ACF 的抑制作用高于饮食猪肝脏 EtnGpl。此外,饮食 EtnGpl 降低了 DMH 诱导的氧化损伤、TNF-α 的过度产生以及结肠黏膜中凋亡相关蛋白的表达。饮食海鞘肌肉 EtnGpl 的作用优于饮食猪肝脏 EtnGpl。我们的结果表明了饮食 PlsEtn 抑制 ACF 形成和细胞凋亡的机制。饮食 PlsEtn 通过减少结肠炎症和氧化应激从而减少 DMH 诱导的肠道损伤来实现这种抑制。这些发现为饮食 PlsEtn 在结肠癌发生过程中的功能作用提供了新的见解。

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