Suppr超能文献

SMOFLipid 对新生豚鼠肺泡发育的影响。

Impact of SMOFLipid on Pulmonary Alveolar Development in Newborn Guinea Pigs.

机构信息

Department of Nutrition, University of Montréal, Montréal, Canada.

Department of Pediatrics-Neonatology, Hospital Sainte-Justine, University of Montréal, Montréal, Canada.

出版信息

JPEN J Parenter Enteral Nutr. 2018 Nov;42(8):1314-1321. doi: 10.1002/jpen.1153. Epub 2018 Mar 13.

Abstract

BACKGROUND

Parenteral nutrition (PN) is associated with bronchopulmonary dysplasia in premature infants. In animals, PN leads to alveolar loss following stimulation of apoptosis by oxidative stress (oxidized redox potential). Peroxides and aldehydes generated in PN can induce hypo-alveolarization. The implication of peroxides, which is reduced by light protection, is demonstrated. The implication of aldehydes from omega-6 fatty acids oxidation is expected. The hypothesis is that composition and light exposure of PN influences bronchopulmonary dysplasia development. Since SMOFLipid (SMOF) contains a lower amount of omega-6 fatty acids than Intralipid (IL), the aim was to compare, the impacts of PN compounded with SMOF or IL, photo-protected or not, on alveolar development.

MATERIALS AND METHODS

Three-day-old Guinea pigs received PN, photo-protected or not, made with SMOF or IL through a jugular vein catheter. After 4 days, lungs were sampled for determinations of redox potential of glutathione, apoptosis (caspase-3, caspase-8, and caspase-9) and alveolarization index (histology: number of intercepts/mm).

RESULTS

Compared with IL, SMOF induces a greater oxidation of redox potential (-200 ± 1 versus [vs] -205 ± 1 mV), apoptosis (caspase-3: 0.27 ± 0.04 vs 0.16 ± 0.02; caspase-9: 0.47 ± 0.03 vs 0.30 ± 0.03), and a lower alveolarization index (27.2 ± 0.8 vs 30.0 ± 0.9). Photo-protection prevented activation of caspase-9 and was statistically without effect on redox potential, caspase-3, and alveolarization index.

CONCLUSION

In our model, SMOF is pro-oxidant and induces hypo-alveolarization following exaggerated apoptosis. These results highlight the need for further studies before introducing SMOFLipid in standard neonatal care.

摘要

背景

肠外营养(PN)与早产儿支气管肺发育不良有关。在动物中,PN 通过氧化应激(氧化还原电位升高)刺激细胞凋亡导致肺泡丧失。PN 中产生的过氧化物和醛类会导致肺泡发育不全。本研究旨在证明光保护可减少过氧化物的影响,并预期 ω-6 脂肪酸氧化产生的醛类也会有影响。假设 PN 的组成和光照暴露会影响支气管肺发育不良的发展。由于 SMOFLipid(SMOF)比 Intralipid(IL)含有更少的 ω-6 脂肪酸,因此本研究旨在比较经颈内静脉导管给予光保护或非光保护的 SMOF 或 IL 复合 PN 对肺泡发育的影响。

材料和方法

3 日龄豚鼠接受 PN,通过颈内静脉导管给予 SMOF 或 IL,光保护或非光保护。4 天后,取肺组织测定谷胱甘肽的氧化还原电位、细胞凋亡(caspase-3、caspase-8 和 caspase-9)和肺泡化指数(组织学:截距/mm 数)。

结果

与 IL 相比,SMOF 诱导更大的氧化还原电位(-200 ± 1 对-205 ± 1 mV)、细胞凋亡(caspase-3:0.27 ± 0.04 对 0.16 ± 0.02;caspase-9:0.47 ± 0.03 对 0.30 ± 0.03)和更低的肺泡化指数(27.2 ± 0.8 对 30.0 ± 0.9)。光保护可防止 caspase-9 的激活,对氧化还原电位、caspase-3 和肺泡化指数无统计学影响。

结论

在我们的模型中,SMOF 是一种促氧化剂,可通过过度的细胞凋亡引起肺泡发育不全。这些结果强调在引入 SMOFLipid 于新生儿常规护理之前,需要进一步研究。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验