Pomegranate seed oil reduces intestinal damage in a rat model of necrotizing enterocolitis
Pomegranate seed oil reduces intestinal damage in a rat model of necrotizing enterocolitis
复制标题
DOI：
10.1152/ajpgi.00248.2012
复制
发表时间：
2012-09-01
影响因子：
4.5
通讯作者：
Dvorak, Bohuslav
中科院分区：
文献类型：
--
作者：
Coursodon-Boyiddle, Christine F.;Snarrenberg, Chelsea L.;Dvorak, Bohuslav
Coursodon-Boyiddle CF，Snarrenberg CL，Adkins-Rieck CK，Bassaganya-Riera J，Hontecillas R，Lawrence P，Brenna JT，Jouni ZE，Dvorak B.在坏死性小肠结肠炎的大鼠模型中，补骨脂籽油减少肠道损伤。美国生理学杂志胃肠和肝脏生理学303：G744-G751，2012年。首次发表于2012年7月19日; doi：10.1152/ajpgi.00248.2012.-石榴籽油（PSO）是石榴酸（普阿）等共轭亚麻酸的主要来源，具有很强的抗炎作用。坏死性小肠结肠炎（NEC）是一种与严重和过度的肠道炎症相关的毁灭性疾病。本研究的目的是评估口服PSO对NEC大鼠模型中NEC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：母鼠喂养（DF），配方饲料喂养的大鼠（FF），或大鼠喂养配方补充1.5%的PSO（FF + PSO）。所有组均暴露于窒息/冷应激以诱导NEC。在末端回肠中评估了肠损伤、上皮细胞增殖、细胞因子产生和三叶因子3（Tff 3）产生。口服PSO（FF + PSO）可使NEC的发生率从61%降至26%。喂食含有PSO的配方改善了损伤部位的肠上皮细胞增殖。在经PSO处理的动物中，FF大鼠回肠中促炎性IL-6、IL-8、IL-12、IL-23和TNF-α水平的升高正常化。FF大鼠中Tff 3的产生与DF相比减少，但不受PSO的进一步影响。总之，在新生大鼠模型中，PSO的给药可防止NEC。这种保护作用与改善肠上皮内稳态和PSO对发育中的肠粘膜的强抗炎作用有关。
Coursodon-Boyiddle CF, Snarrenberg CL, Adkins-Rieck CK, Bassaganya-Riera J, Hontecillas R, Lawrence P, Brenna JT, Jouni ZE, Dvorak B. Pomegranate seed oil reduces intestinal damage in a rat model of necrotizing enterocolitis. Am J Physiol Gastrointest Liver Physiol 303: G744-G751, 2012. First published July 19, 2012; doi:10.1152/ajpgi.00248.2012.-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-alpha 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.