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饲粮木寡糖通过内质网-线粒体系统途径缓解仔猪 LPS 诱导的肠道损伤。

Dietary xylo-oligosaccharides alleviates LPS-induced intestinal injury via endoplasmic reticulum-mitochondrial system pathway in piglets.

机构信息

Institute of Animal Nutrition, Sichuan Agricultural University, Chengdu, Sichuan, China.

Key Laboratory for Animal Disease-Resistance Nutrition of China Ministry of Education, Chengdu, Sichuan, China.

出版信息

J Anim Sci. 2024 Jan 3;102. doi: 10.1093/jas/skae238.

Abstract

The beneficial effects of xylo-oligosaccharides (XOS) on the intestine have been widely reported, including anti-inflammation, antioxidant, maintenance of intestinal epithelial barrier, and treatment of intestinal injury. However, the specific mechanism of XOS in mitigating intestinal injury in weaned piglets remains unclear. Therefore, this study aimed to explore the specific mechanism of XOS in mitigating intestinal injury. The study is a complete randomized design with 24 weaned piglets in a 2 × 2 factorial arrangement that includes diet treatments (basal diet vs. 0.02% XOS) and immunological challenge [saline vs. lipopolysaccharide (LPS)]. All piglets were fed a basal diet or a XOS diet for 21 d. On day 22, all piglets received an injection of LPS or saline. In this study, dietary XOS increased jejunal villus height, reduced crypt depth and oxidative stress, and enhanced the gene and protein expression of Claudin-1, Occludin, and zonula occludens 1 (P < 0.05). The piglets fed the XOS diet had lower serum Diamine oxidase activity and d-lactic acid content (P < 0.05). In addition, dietary XOS regulates endoplasmic reticulum (ER)-mitochondria system function and the expression of key molecules, including mitochondrial dynamics dysfunction [mitofusin (Mfn)-1, optic atrophy 1, fission 1, and dynamin-related protein 1], ER stress [activating transcription factor 4 (ATF4), ATF6, C/EBP-homologous protein, eukaryotic initiation factor 2α, glucose-regulated protein (GRP) 78, GRP94, and protein kinase R-like ER kinase] and the mitochondria-associated ER membranes (MAM) disorders (Mfn2, GRP75, and voltage-dependent anion channel 1) (P < 0.05). Therefore, the findings to indicate that dietary XOS is effective against LPS-induced jejunal injury may be attributed to its ability to alleviate mitochondrial dynamics dysfunction, ER stress, and MAM disorders.

摘要

木寡糖(XOS)对肠道的有益影响已被广泛报道,包括抗炎、抗氧化、维持肠道上皮屏障和治疗肠道损伤。然而,XOS 减轻断奶仔猪肠道损伤的具体机制尚不清楚。因此,本研究旨在探讨 XOS 减轻肠道损伤的具体机制。该研究采用完全随机设计,24 头断奶仔猪采用 2×2 因子设计,包括饮食处理(基础日粮与 0.02%XOS)和免疫挑战[生理盐水与脂多糖(LPS)]。所有仔猪均饲喂基础日粮或 XOS 日粮 21d。第 22 天,所有仔猪均接受 LPS 或生理盐水注射。在本研究中,饲粮 XOS 增加了空肠绒毛高度,降低了隐窝深度和氧化应激,并增强了 Claudin-1、Occludin 和 zonula occludens 1 的基因和蛋白表达(P<0.05)。饲喂 XOS 日粮的仔猪血清二胺氧化酶活性和 D-乳酸含量较低(P<0.05)。此外,饲粮 XOS 调节内质网(ER)-线粒体系统功能和关键分子的表达,包括线粒体动力学障碍[融合蛋白 1(Mfn-1)、视神经萎缩蛋白 1、分裂 1 和动力相关蛋白 1]、内质网应激[激活转录因子 4(ATF4)、ATF6、C/EBP 同源蛋白、真核起始因子 2α、葡萄糖调节蛋白(GRP)78、GRP94 和蛋白激酶 R 样内质网激酶]和线粒体相关内质网膜(MAM)紊乱(Mfn2、GRP75 和电压依赖性阴离子通道 1)(P<0.05)。因此,饲粮 XOS 对 LPS 诱导的空肠损伤有效,可能归因于其缓解线粒体动力学障碍、内质网应激和 MAM 紊乱的能力。

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