Akdagli Seden, Williams Ryan A, Kim Hyun J, Yan Yuling, Mustapha Mirna, Most Sam P
Division of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Plast Reconstr Surg Glob Open. 2016 Dec 23;4(12):e1186. doi: 10.1097/GOX.0000000000001186. eCollection 2016 Dec.
Understanding the mechanisms in nerve damage can lead to better outcomes for neuronal rehabilitation. The purpose of our study was to assess the effect of major histocompatibility complex I deficiency and inhibition of the classical complement pathway (C1q) on functional recovery and cell survival in the facial motor nucleus (FMN) after crush injury in adult and juvenile mice.
A prospective blinded analysis of functional recovery and cell survival in the FMN after a unilateral facial nerve crush injury in juvenile and adult mice was undertaken between wild-type, C1q knockout (C1q-/-), and KbDb knockout (KbDb-/-) groups. Whisker function was quantified to assess functional recovery. Neuron counts were performed to determine neuron survival in the FMN after recovery.
After facial nerve injury, all adult wild-type mice fully recovered. Juvenile mice recovered incompletely corresponding to a greater neuron loss in the FMN of juveniles compared with adults. The C1q-/- juvenile and adult groups did not differ from wild type. The KbDb-/- adults demonstrated 50% recovery of whisker movement and decreased cell survival in FMN. The KbDb-/- juvenile group did not demonstrate any difference from control group.
Histocompatibility complex I plays a role for neuroprotection and enhanced facial nerve recovery in adult mice. Inhibition of the classical complement pathway alone does not affect functional recovery or neuronal survival. The alternative and mannose binding pathways pose alternative means for activating the final components of the pathway that may lead to acute nerve damage.
了解神经损伤机制有助于改善神经元康复效果。我们研究的目的是评估主要组织相容性复合体I缺陷和经典补体途径（C1q）抑制对成年和幼年小鼠面神经挤压伤后面部运动核（FMN）功能恢复和细胞存活的影响。
对野生型、C1q基因敲除（C1q-/-）和KbDb基因敲除（KbDb-/-）组的幼年和成年小鼠单侧面神经挤压伤后的FMN功能恢复和细胞存活进行前瞻性盲法分析。通过量化触须功能来评估功能恢复情况。在恢复后进行神经元计数以确定FMN中的神经元存活情况。
面神经损伤后，所有成年野生型小鼠均完全恢复。幼年小鼠恢复不完全，与成年小鼠相比，幼年小鼠FMN中的神经元损失更大。C1q-/-幼年和成年组与野生型无差异。KbDb-/-成年小鼠触须运动恢复50%，FMN中的细胞存活率降低。KbDb-/-幼年组与对照组无差异。
主要组织相容性复合体I在成年小鼠的神经保护和增强面神经恢复中发挥作用。单独抑制经典补体途径不影响功能恢复或神经元存活。替代途径和甘露糖结合途径为激活可能导致急性神经损伤的途径的最终成分提供了替代方式。
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