低聚木糖(XOS)对肠道的有益作用已被广泛报道,包括抗炎,抗氧化剂,维持肠上皮屏障,以及肠道损伤的治疗。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。该研究是一项完整的随机设计,对24只断奶仔猪进行2×2阶乘排列,其中包括饮食处理(基础饮食vs0.02%XOS)和免疫挑战[盐水vs脂多糖(LPS)]。所有仔猪饲喂基础日粮或XOS日粮21天。在第22天,所有仔猪接受LPS或盐水注射。在这项研究中,饮食XOS增加空肠绒毛高度,降低隐窝深度和氧化应激,并增强了Claudin-1,Occludin的基因和蛋白质表达,和小带闭塞1(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,膳食XOS调节内质网(ER)-线粒体系统功能和关键分子的表达,包括线粒体动力学功能障碍[mitofusin(Mfn)-1,视神经萎缩1,裂变1和动力蛋白相关蛋白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]和线粒体相关的ER膜(MAM)疾病(Mfn2,GRP75和电压负离子通道1)(P<0.05)。因此,研究结果表明,膳食XOS是有效对抗LPS诱导的空肠损伤可能归因于其减轻线粒体动力学功能障碍的能力,ER压力,和MAM障碍。
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.