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消化早期早产儿人乳可抑制肿瘤坏死因子诱导的肠上皮细胞炎症和细胞毒性。

Digested Early Preterm Human Milk Suppresses Tumor Necrosis Factor-induced Inflammation and Cytotoxicity in Intestinal Epithelial Cells.

机构信息

UIC Department of Kinesiology and Nutrition.

Department of Pediatrics, Rush University Medical Center.

出版信息

J Pediatr Gastroenterol Nutr. 2018 Jun;66(6):e153-e157. doi: 10.1097/MPG.0000000000001932.

Abstract

OBJECTIVES

The aim of this study was to determine the effect of digested whole human milk (HM; first sample available after birth from mothers of premature infants) on inflammation, oxidative stress, and cytotoxicity in Caco-2 human intestinal epithelial cells stimulated with lipopolysaccharides or tumor necrosis factor (TNF) to mimic the potential in vivo insults facing the premature infant's gastrointestinal tract.

METHODS

Fully differentiated Caco-2 cells were exposed to digested HM (n = 10; samples from 10 different individuals) before stimulation with lipopolysaccharides, TNF, or no stimulation overnight. Inflammation was determined by production of interleukin-8, oxidative stress by levels of F2-isoprostane, and cytotoxicity by released lactate dehydrogenase.

RESULTS

HM significantly suppressed interleukin-8 production and cytotoxicity in TNF-stimulated cells, while also suppressing cell death under baseline conditions. Individual HM samples differed widely in their ability to modulate cellular responses.

CONCLUSIONS

Results from this study provide evidence that digested HM can reduce both an exaggerated inflammatory response and intestinal damage that contribute to the pathogenesis of necrotizing enterocolitis.

摘要

目的

本研究旨在确定消化全人乳(HM;早产儿母亲出生后最早获得的第一份母乳样本)对脂多糖或肿瘤坏死因子(TNF)刺激的 Caco-2 人肠上皮细胞炎症、氧化应激和细胞毒性的影响,以模拟早产儿胃肠道可能面临的潜在体内损伤。

方法

完全分化的 Caco-2 细胞在与脂多糖、TNF 或无刺激孵育过夜之前接受消化 HM(n = 10;来自 10 个不同个体的样本)处理。通过白细胞介素-8 的产生来确定炎症,通过 F2-异前列腺素水平来确定氧化应激,通过释放的乳酸脱氢酶来确定细胞毒性。

结果

HM 可显著抑制 TNF 刺激细胞中白细胞介素-8 的产生和细胞毒性,同时在基线条件下也抑制细胞死亡。个体 HM 样本在调节细胞反应的能力上差异很大。

结论

本研究结果提供了证据表明,消化 HM 可减少导致坏死性小肠结肠炎发病机制的过度炎症反应和肠道损伤。

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