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Dietary xylo-oligosaccharides alleviates LPS-induced intestinal injury via endoplasmic reticulum-mitochondrial system pathway in piglets
Journal of Animal Science ( IF 2.7 ) Pub Date : 2024-08-15 , DOI: 10.1093/jas/skae238
Guangmang Liu 1 , Weixiao Sun 1 , Ruinan Zhang 1 , Fei Shen 2 , Gang Jia 1 , Hua Zhao 1 , Xiaoling Chen 1 , Jing Wang 3
Affiliation  

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 days. 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-dlependent 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

中文翻译:


日粮低聚木糖通过内质网-线粒体系统途径减轻脂多糖诱导的仔猪肠道损伤



低聚木糖(XOS)对肠道的有益作用已被广泛报道,包括抗炎、抗氧化、维持肠上皮屏障和治疗肠道损伤。然而,低聚木糖减轻断奶仔猪肠道损伤的具体机制仍不清楚。因此,本研究旨在探讨低聚木糖减轻肠道损伤的具体机制。该研究是一项完全随机设计,24 头断奶仔猪采用 2 × 2 因子排列,包括饮食治疗(基础饮食 vs 0.02% XOS)和免疫挑战 [盐水 vs 脂多糖 (LPS)]。所有仔猪均饲喂基础日粮或低聚木糖日粮 21 天。第 22 天,所有仔猪均注射 LPS 或盐水。在这项研究中,膳食低聚木糖增加了空肠绒毛高度,减少了隐窝深度和氧化应激,并增强了 Claudin-1、Occludin 和闭合小带 1 的基因和蛋白表达(P < 0.05)。饲喂低聚木糖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,膳食低聚木糖调节内质网(ER)-线粒体系统功能和关键分子的表达,包括线粒体动力学功能障碍[线粒体融合蛋白(Mfn)-1、视神经萎缩1、裂变1和动力相关蛋白1]、ER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 ER 激酶] 和线粒体相关 ER 膜( MAM) 疾病(Mfn2、GRP75 和电压依赖性阴离子通道 1)(P < 0.05)。因此,研究结果表明膳食低聚木糖能有效对抗 LPS 引起的空肠损伤,这可能归因于其缓解线粒体动力学功能障碍、ER 应激和 MAM 疾病的能力
更新日期:2024-08-15
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