Cai Jing, Li Liheng, Song Yongdong, Xu Lei, Mao Yanyan, Wang Haibo
Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial ENT Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Department of Otolaryngology, The First Affiliated Hospital of Huzhou University, Zhejiang, China.
ORL J Otorhinolaryngol Relat Spec. 2021;83(6):449-456. doi: 10.1159/000514994. Epub 2021 May 7.
This study aimed to investigate the potential neuroprotective action of brimonidine against facial nerve crush injury in rats and the possible underlying mechanisms.
Sixty Wistar adult rats were randomly and equally divided into 3 groups: 40 rats underwent unilateral facial nerve crush injury and were administered with either saline (intraperitoneal, n = 20) or brimonidine 1 mg/kg/day (intraperitoneal, n = 20) for 5 consecutive days. Functional and electromyographic recovery was recorded postoperatively. The facial nucleus of 5 mice in each group was analyzed for mRNA expression levels of GFAP, PAF, NT-4, P75NTR, NF-κB, TNF-α, IL-6, and α2-ARs by qRT-PCR.
Brimonidine promoted the recovery of vibrissae movement, eyelid closure, and electrophysiological function in a rat model of nerve crush injury. Hematoxylin and eosin staining and electron microscopy showed significant recovery of Schwann cells and axons in the brimonidine group. Brimonidine attenuated the crush-induced upregulation in GFAP and PAF mRNA (p < 0.05), as well as enhanced the mRNA levels of NT-4 and P75NTR (p < 0.05), while decreased the expression of NF-κB, TNF-α and IL-6 (p < 0.05).
Brimonidine could promote the recovery of facial nerve crush injury in rats via suppressing of GFAP/PAF activation and neuroinflammation and increasing neurotrophic factors. Brimonidine may be apromising candidate agent for the treatment of facial nerve injury.
本研究旨在探讨溴莫尼定对大鼠面神经挤压伤的潜在神经保护作用及其可能的潜在机制。
60只成年Wistar大鼠随机等分为3组：40只大鼠接受单侧面神经挤压伤，连续5天腹腔注射生理盐水（n = 20）或1 mg/kg/天溴莫尼定（n = 20）。术后记录功能和肌电图恢复情况。通过qRT-PCR分析每组5只小鼠面神经核中GFAP、PAF、NT-4、P75NTR、NF-κB、TNF-α、IL-6和α2-ARs的mRNA表达水平。
在神经挤压伤大鼠模型中，溴莫尼定促进了触须运动、眼睑闭合和电生理功能的恢复。苏木精-伊红染色和电子显微镜显示溴莫尼定组雪旺细胞和轴突有明显恢复。溴莫尼定减弱了挤压诱导的GFAP和PAF mRNA上调（p < 0.05），同时提高了NT-4和P75NTR的mRNA水平（p < 0.05），而降低了NF-κB、TNF-α和IL-6的表达（p < 0.05）。
溴莫尼定可通过抑制GFAP/PAF激活和神经炎症以及增加神经营养因子来促进大鼠面神经挤压伤的恢复。溴莫尼定可能是治疗面神经损伤的一种有前景的候选药物。
