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新型吞咽困难大鼠模型中的周围神经再生。

Peripheral Nerve Regeneration in a Novel Rat Model of Dysphagia.

机构信息

Department of Oral and Maxillofacial Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Division of Reconstructive Surgery for Oral and Maxillofacial Region, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

出版信息

Methods Mol Biol. 2020;2155:107-113. doi: 10.1007/978-1-0716-0655-1_9.

Abstract

The superior laryngeal nerve (SLN) is known to play an essential role in the laryngeal reflex and swallowing. Damage to the SLN causes difficulty swallowing, that is, dysphagia. We successfully developed a novel rat model of dysphagia by SLN injury, in which we could evaluate the neuroregenerative capacity of stem cell from human exfoliated deciduous teeth (SHED). The dysphagic rats exhibit weight loss and altered drinking patterns. Furthermore, SLN injury induces a delayed onset of the swallowing reflex and accumulation of laryngeal debris in the pharynx. This rat model was used to evaluate the systemic application of SHED-conditioned medium (SHED-CM) as a therapeutic candidate for dysphagia. We found that SHED-CM promoted functional recovery and significant axonal regeneration in SLNs through the polarization shift of macrophages from activated inflammatory macrophages (M1) to anti-inflammatory macrophages (M2) and angiogenesis. This chapter describes the establishment of SLN-injury induced dysphagia rat model and the preparation and application of SHED-CM.

摘要

喉上神经 (SLN) 在喉反射和吞咽中起着至关重要的作用。SLN 损伤会导致吞咽困难,即吞咽困难。我们通过 SLN 损伤成功开发了一种新型的大鼠吞咽困难模型,在此模型中,我们可以评估人脱落乳牙源性干细胞 (SHED) 的神经再生能力。吞咽困难的大鼠表现出体重减轻和饮水模式改变。此外,SLN 损伤会导致吞咽反射延迟出现,并在咽部积聚喉部分泌物。该大鼠模型用于评估 SHED 条件培养基 (SHED-CM) 作为吞咽困难治疗候选物的全身应用。我们发现,SHED-CM 通过将巨噬细胞从激活的炎症性巨噬细胞 (M1) 向抗炎性巨噬细胞 (M2) 和血管生成的极化转变,促进 SLN 中的功能恢复和显著的轴突再生。本章描述了 SLN 损伤诱导的吞咽困难大鼠模型的建立以及 SHED-CM 的制备和应用。

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