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用于研究早产弥漫性白质损伤机制的转化小鼠模型。

A translational mouse model for investigation of the mechanism of preterm diffuse white matter injury.

作者信息

Chen Qiufan, Zhang Ke, Wang Minjie, Gao Ruiwei, Wang Qian, Xiao Mili, Chen Chao

机构信息

Department of Neonatology, Children's Hospital of Fudan University, Shanghai, China.

Key Laboratory of Neonatal Disease, Ministry of Health, Shanghai, China.

出版信息

Transl Pediatr. 2022 Jul;11(7):1074-1084. doi: 10.21037/tp-22-58.

Abstract

BACKGROUND

The increasing incidence of preterm birth has led to a global problem of adverse neurodevelopmental outcomes in preterm neonates as a result of brain injury. There is still a lack of models mimicking diffuse white matter injury (WMI) in preterm neonates that can be applied to transgenic mice.

METHODS

The right common carotid artery of the neonatal mouse was ligated on postnatal day 3 (P3) C57BL/6 mice and followed by 80, 90, or 100 min of hypoxia using a mixture of 10%±0.2% oxygen-nitrogen. The most suitable model was chosen by characterizing the effects of this hypoxic-ischemic insult on development of myelin, glial cell conditions, and neurological outcomes by hematoxylin-eosin (HE) staining performed at postnatal day 17 (P17), western blot measuring myelin basic protein (MBP) at postnatal day 10 (P10) and P17, immunofluorescence staining of MBP-neurofilament protein heavy chain (NFH), oligodendrocyte transcription factor-2 (Olig2)-adenomatous polyposis coli clone (CC1), glial fibrillary acidic protein (GFAP) and ionic calcium linker protein (Iba-1) at P17, electron microscopy observing myelin microstructure at postnatal day 52 (P52) and behavioral testing at postnatal day 45-50 (P45-P50).

RESULTS

The 90-min group showed neuroanatomical changes in the ipsilateral side of the brain, the 80-min group showed minor changes, and the 100-min group showed severe injury. Mice in the 90-min group subsequently showed marked activation of astrocytes, augmentation of microglia, a notable decrease in expression of MBP with a normal level of NFH, long-term cognitive dysfunction, and impairment of the myelin ultrastructure in adulthood.

CONCLUSIONS

In conclusion, a mouse model of preterm diffuse WMI rather than cystic periventricular leukomalacia was successfully achieved by ligating one of the common carotid arteries on P3 followed by 90 min of hypoxia in a mixture of 10%±0.2% oxygen-nitrogen. The attempt provides an adequate translational animal model for elucidating the underlying mechanism.

摘要

背景

早产发生率的上升已导致早产新生儿因脑损伤出现不良神经发育结局这一全球性问题。目前仍缺乏可应用于转基因小鼠的、模拟早产新生儿弥漫性白质损伤(WMI)的模型。

方法

在出生后第3天(P3)结扎C57BL/6新生小鼠的右侧颈总动脉,然后使用10%±0.2%氧气 - 氮气混合气体进行80、90或100分钟的缺氧处理。通过在出生后第17天(P17)进行苏木精 - 伊红(HE)染色来表征这种缺氧缺血性损伤对髓鞘发育、神经胶质细胞状况和神经学结局的影响,在出生后第10天(P10)和P17通过蛋白质免疫印迹法检测髓鞘碱性蛋白(MBP),在P17对MBP - 神经丝蛋白重链(NFH)、少突胶质细胞转录因子 - 2(Olig2) - 腺瘤性息肉病大肠杆菌克隆(CC1)、胶质纤维酸性蛋白(GFAP)和离子钙连接蛋白(Iba - 1)进行免疫荧光染色,在出生后第52天(P52)通过电子显微镜观察髓鞘微观结构,并在出生后第45 - 50天(P45 - P50)进行行为测试,从而选择最合适的模型。

结果

90分钟组在脑的同侧显示神经解剖学变化,80分钟组变化较小,100分钟组显示严重损伤。90分钟组的小鼠随后显示星形胶质细胞明显活化、小胶质细胞增多、MBP表达显著降低而NFH水平正常、长期认知功能障碍以及成年期髓鞘超微结构受损。

结论

总之,通过在P3结扎一条颈总动脉,然后在10%±0.2%氧气 - 氮气混合气体中进行90分钟缺氧处理,成功建立了早产弥漫性WMI而非囊性脑室周围白质软化的小鼠模型。该尝试为阐明潜在机制提供了合适的转化动物模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8667/9360811/2334b2a45481/tp-11-07-1074-f1.jpg

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