Department of Pediatrics, Gaziosmanpasa Universitesi, Tokat, Turkey.
Department of Neonatology, Gaziosmanpasa Universitesi, Tokat, Turkey.
J Matern Fetal Neonatal Med. 2021 Nov;34(22):3761-3767. doi: 10.1080/14767058.2020.1818210. Epub 2020 Sep 20.
The pathophysiology of necrotizing enterocolitis (NEC) includes the massive production of endogenous cytokines with exaggerated activation of inflammatory pathways. Ursodeoxycholic acid (UDCA) has been used as an anti-inflammatory, antioxidant, and anti-apoptotic agent. We investigated the possible protective effects of UDCA in a neonatal rat pup model of NEC.
We randomly divided rat pups into three groups: a control group, a non-treated NEC group, and a UDCA-treated NEC group. We induced NEC by feeding formula enterally and hypoxia/reoxygenation. Intestinal samples were collected for histopathological and immunohistochemical evaluation. Blood samples were taken for biochemical analyses.
UDCA significantly reduced the extents of terminal ileal and jejunal injuries compared to the NEC group ( < .01), reduced Bax and caspase-3 immunoreactivities (both < .01), and lowered serum levels of platelet-activating factor and intestinal fatty acid-binding protein ( < .01, = .023, respectively).
In a rat model of NEC, UDCA protects against adverse intestinal histological, immunohistochemical, and biochemical changes. UDCA significantly reduces the effects of NEC on the rat pup intestine.
坏死性小肠结肠炎（NEC）的病理生理学包括内源性细胞因子的大量产生，以及炎症途径的过度激活。熊去氧胆酸（UDCA）已被用作抗炎、抗氧化和抗凋亡剂。我们研究了 UDCA 在新生大鼠 NEC 模型中的可能保护作用。
我们将大鼠幼崽随机分为三组：对照组、未治疗的 NEC 组和 UDCA 治疗的 NEC 组。我们通过肠内喂养配方和缺氧/复氧来诱导 NEC。采集肠组织样本进行组织病理学和免疫组织化学评估。采集血样进行生化分析。
与 NEC 组相比，UDCA 显著降低了回肠和空肠末端的损伤程度（<0.01），降低了 Bax 和 caspase-3 的免疫反应性（均<0.01），并降低了血小板激活因子和肠脂肪酸结合蛋白的血清水平（<0.01，=0.023）。
在 NEC 大鼠模型中，UDCA 可预防肠道组织学、免疫组织化学和生化的不良变化。UDCA 可显著减轻 NEC 对大鼠幼崽肠道的影响。
