College of Animal Science & Technology, Nanjing Agricultural University, Nanjing 210095, China.
Postdoctoral Research Station of Clinical Veterinary Medicine, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, China 210095.
Oxid Med Cell Longev. 2020 Oct 10;2020:7178123. doi: 10.1155/2020/7178123. eCollection 2020.
Intrauterine growth retardation (IUGR) delays the gut development of neonates, but effective treatment strategies are still limited. This study used newborn piglets as a model to evaluate the protective effect of polydatin (PD) against IUGR-induced intestinal injury. In total, 36 IUGR piglets and an equal number of normal birth weight (NBW) littermates were fed either a basal diet or a PD-supplemented diet from 21 to 35 days of age. Compared with NBW, IUGR induced jejunal damage and barrier dysfunction of piglets, as indicated by observable bacterial translocation, enhanced apoptosis, oxidative and immunological damage, and mitochondrial dysfunction. PD treatment decreased bacterial translocation and inhibited the IUGR-induced increases in circulating diamine oxidase activity ( = 0.039) and D-lactate content ( = 0.004). The apoptotic rate ( = 0.024) was reduced by 35.2% in the PD-treated piglets, along with increases in villus height ( = 0.033) and in ratio of villus height to crypt depth ( = 0.049). PD treatment promoted superoxide dismutase ( = 0.026) and glutathione S-transferase activities ( = 0.006) and reduced malondialdehyde ( = 0.015) and 8-hydroxy-2'-deoxyguanosine accumulation ( = 0.034) in the jejunum. The PD-treated IUGR piglets showed decreased jejunal myeloperoxidase activity ( = 0.029) and tumor necrosis factor alpha content ( = 0.035) than those received a basal diet. PD stimulated nuclear sirtuin 1 ( = 0.028) and mitochondrial citrate synthase activities ( = 0.020) and facilitated adenosine triphosphate production ( = 0.009) in the jejunum of piglets. Furthermore, PD reversed the IUGR-induced declines in mitochondrial DNA content ( = 0.048), the phosphorylation of adenosine monophosphate-activated protein kinase alpha ( = 0.027), and proliferation-activated receptor gamma coactivator 1 alpha expression ( = 0.033). Altogether, the results indicate that PD may improve jejunal integrity, mitigate mucosal oxidative and immunological damage, and facilitate mitochondrial function in IUGR piglets.
宫内发育迟缓（IUGR）延迟了新生儿的肠道发育，但有效的治疗策略仍然有限。本研究使用新生仔猪作为模型，评估白藜芦醇（PD）对 IUGR 诱导的肠道损伤的保护作用。总共 36 头 IUGR 仔猪和等量的正常出生体重（NBW）同窝仔猪从 21 日龄到 35 日龄分别给予基础日粮或 PD 补充日粮。与 NBW 相比，IUGR 诱导仔猪空肠损伤和屏障功能障碍，表现为明显的细菌易位、增强的凋亡、氧化和免疫损伤以及线粒体功能障碍。PD 处理减少了细菌易位，并抑制了 IUGR 诱导的循环二胺氧化酶活性（=0.039）和 D-乳酸含量（=0.004）的增加。PD 处理组仔猪的凋亡率降低了 35.2%（=0.024），绒毛高度（=0.033）和绒毛高度与隐窝深度的比值（=0.049）增加。PD 处理促进了超氧化物歧化酶（=0.026）和谷胱甘肽 S-转移酶的活性（=0.006），并减少了空肠中二醛（=0.015）和 8-羟基-2'-脱氧鸟苷的积累（=0.034）。与接受基础日粮的 IUGR 仔猪相比，PD 处理的 IUGR 仔猪空肠髓过氧化物酶活性（=0.029）和肿瘤坏死因子-α含量（=0.035）降低。PD 刺激核 Sirtuin 1（=0.028）和线粒体柠檬酸合酶的活性（=0.020），并促进空肠中三磷酸腺苷的产生（=0.009）。此外，PD 逆转了 IUGR 诱导的线粒体 DNA 含量下降（=0.048）、腺苷单磷酸激活蛋白激酶-α的磷酸化（=0.027）和增殖激活受体 γ共激活因子 1α表达（=0.033）。总之，这些结果表明 PD 可能改善 IUGR 仔猪空肠完整性，减轻黏膜氧化和免疫损伤，并促进线粒体功能。
