Neuroprotective Effect of Brimonidine against Facial Nerve Crush Injury in Rats via Suppressing GFAP/PAF Activation and Neuroinflammation

Abstract

<b><i>Objective:</i></b> This study aimed to investigate the potential neuroprotective action of brimonidine against facial nerve crush injury in rats and the possible underlying mechanisms. <b><i>Methods:</i></b> 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, <i>n</i> = 20) or brimonidine 1 mg/kg/day (intraperitoneal, <i>n</i> = 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, P75^NTR, NF-κB, TNF-α, IL-6, and α₂-ARs by qRT-PCR. <b><i>Results:</i></b> 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 (<i>p</i> &#x3c; 0.05), as well as enhanced the mRNA levels of NT-4 and P75^NTR (<i>p</i> &#x3c; 0.05), while decreased the expression of NF-κB, TNF-α and IL-6 (<i>p</i> &#x3c; 0.05). <b><i>Conclusions:</i></b> 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.