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本文引用的文献

1
Innate Immunity in the Small Intestine of the Preterm Infant.早产儿小肠中的先天性免疫
Neoreviews. 2011 Sep 1;12(9):e517-e526. doi: 10.1542/neo.12-9-e517.
2
Conjugated linoleic acid modulates immune responses in patients with mild to moderately active Crohn's disease.共轭亚油酸可调节轻至中度活动期克罗恩病患者的免疫应答。
Clin Nutr. 2012 Oct;31(5):721-7. doi: 10.1016/j.clnu.2012.03.002. Epub 2012 Apr 20.
3
Necrotising enterocolitis is characterised by disrupted immune regulation and diminished mucosal regulatory (FOXP3)/effector (CD4, CD8) T cell ratios.坏死性小肠结肠炎的特征是免疫调节紊乱和黏膜调节性(FOXP3)/效应(CD4、CD8)T 细胞比值降低。
Gut. 2013 Jan;62(1):73-82. doi: 10.1136/gutjnl-2011-301551. Epub 2012 Jan 20.
4
Branched chain fatty acids reduce the incidence of necrotizing enterocolitis and alter gastrointestinal microbial ecology in a neonatal rat model.支链脂肪酸可降低新生大鼠坏死性小肠结肠炎的发生率,并改变其胃肠道微生物生态。
PLoS One. 2011;6(12):e29032. doi: 10.1371/journal.pone.0029032. Epub 2011 Dec 14.
5
Activation of PPARγ and δ by dietary punicic acid ameliorates intestinal inflammation in mice.日粮中的 punicic 酸通过激活 PPARγ 和 δ来改善小鼠的肠道炎症。
Br J Nutr. 2011 Sep;106(6):878-86. doi: 10.1017/S0007114511001188. Epub 2011 May 31.
6
Interleukin-23 and T helper 17-type responses in intestinal inflammation: from cytokines to T-cell plasticity.白细胞介素-23 与肠道炎症中的辅助性 T 细胞 17 型反应:从细胞因子到 T 细胞可塑性。
Immunology. 2011 Aug;133(4):397-408. doi: 10.1111/j.1365-2567.2011.03454.x. Epub 2011 Jun 2.
7
Gram negative bacteria are associated with the early stages of necrotizing enterocolitis.革兰氏阴性菌与坏死性小肠结肠炎的早期阶段有关。
PLoS One. 2011 Mar 22;6(3):e18084. doi: 10.1371/journal.pone.0018084.
8
The mechanism of excessive intestinal inflammation in necrotizing enterocolitis: an immature innate immune response.坏死性小肠结肠炎中肠道炎症过度的机制:不成熟的固有免疫反应。
PLoS One. 2011 Mar 21;6(3):e17776. doi: 10.1371/journal.pone.0017776.
9
Pomegranate seed oil, a rich source of punicic acid, prevents diet-induced obesity and insulin resistance in mice.石榴籽油富含 punicalagin,可预防小鼠的饮食诱导肥胖和胰岛素抵抗。
Food Chem Toxicol. 2011 Jun;49(6):1426-30. doi: 10.1016/j.fct.2011.03.037. Epub 2011 Mar 31.
10
Necrotizing enterocolitis.坏死性小肠结肠炎
N Engl J Med. 2011 Jan 20;364(3):255-64. doi: 10.1056/NEJMra1005408.

石榴籽油可减轻坏死性小肠结肠炎大鼠模型的肠道损伤。

Pomegranate seed oil reduces intestinal damage in a rat model of necrotizing enterocolitis.

机构信息

Department of Pediatrics, The University of Arizona, Tucson, 85724-5073, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2012 Sep 15;303(6):G744-51. doi: 10.1152/ajpgi.00248.2012. Epub 2012 Jul 19.

DOI:10.1152/ajpgi.00248.2012
PMID:22821948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3468537/
Abstract

Pomegranate seed oil (PSO), which is the major source of conjugated linolenic acids such as punicic acid (PuA), exhibits strong anti-inflammatory properties. Necrotizing enterocolitis (NEC) is a devastating disease associated with severe and excessive intestinal inflammation. The aim of this study was to evaluate the effects of orally administered PSO on the development of NEC, intestinal epithelial proliferation, and cytokine regulation in a rat model of NEC. Premature rats were divided into three groups: dam fed (DF), formula-fed rats (FF), or rats fed with formula supplemented with 1.5% of PSO (FF + PSO). All groups were exposed to asphyxia/cold stress to induce NEC. Intestinal injury, epithelial cell proliferation, cytokine production, and trefoil factor 3 (Tff3) production were evaluated in the terminal ileum. Oral administration of PSO (FF+PSO) decreased the incidence of NEC from 61 to 26%. Feeding formula with PSO improved enterocyte proliferation in the site of injury. Increased levels of proinflammatory IL-6, IL-8, IL-12, IL-23, and TNF-α in the ileum of FF rats were normalized in PSO-treated animals. Tff3 production in the FF rats was reduced compared with DF but not further affected by the PSO. In conclusion, administration of PSO protects against NEC in the neonatal rat model. This protective effect is associated with an improvement of intestinal epithelial homeostasis and a strong anti-inflammatory effect of PSO on the developing intestinal mucosa.

摘要

石榴籽油(PSO)是共轭亚油酸(如 pun 酸(PuA))的主要来源,具有很强的抗炎特性。坏死性小肠结肠炎(NEC)是一种与严重和过度肠道炎症相关的破坏性疾病。本研究旨在评估口服 PSO 对 NEC 大鼠模型中 NEC 的发展、肠上皮细胞增殖和细胞因子调节的影响。早产大鼠分为三组:母乳喂养组(DF)、配方奶喂养组(FF)或添加 1.5% PSO 的配方奶喂养组(FF+PSO)。所有组均暴露于窒息/冷应激以诱导 NEC。在末端回肠评估肠道损伤、上皮细胞增殖、细胞因子产生和三叶因子 3(Tff3)产生。口服 PSO(FF+PSO)将 NEC 的发生率从 61%降低到 26%。PSO 喂养的配方奶改善了损伤部位的肠细胞增殖。FF 大鼠回肠中促炎细胞因子 IL-6、IL-8、IL-12、IL-23 和 TNF-α 的水平升高,在 PSO 治疗的动物中得到了正常化。与 DF 相比,FF 大鼠的 Tff3 产生减少,但 PSO 对其没有进一步影响。总之,PSO 对新生大鼠 NEC 模型具有保护作用。这种保护作用与改善肠道上皮细胞稳态以及 PSO 对发育中的肠黏膜的强烈抗炎作用有关。