Iwata Shinji, Yamada Hiroyuki, Teraoka Masato, Tanaka Takemichi, Kimura Takuya, Joko Tomonori, Tabata Yasuhiko, Wakisaka Hiroyuki, Hato Naohito
Department of Otolaryngology, Head and Neck Surgery, Ehime University Graduate School of Medicine, Toon, Japan.
Laboratory of Biomaterials, Department of Regeneration Science and Engineering Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan.
PLoS One. 2025 Feb 6;20(2):e0312357. doi: 10.1371/journal.pone.0312357. eCollection 2025.
Severe axonal damage in the peripheral nerves results in retrograde degeneration towards the central side, leading to neuronal cell death, eventually resulting in incomplete axonal regeneration and functional recovery. Therefore, it is necessary to evaluate the facial nerve nucleus in models of facial paralysis, and investigate the efficacy of treatments, to identify treatment options for severe paralysis. Consequently, we aimed to examine the percentage of facial nerve cell reduction and the extent to which intratympanic administration of a basic fibroblast growth factor (bFGF) inhibits neuronal cell death in a model of severe facial paralysis. A severe facial paralysis model was induced in Hartley guinea pigs by freezing the facial canal. Animals were divided into two groups: one group was treated with gelatin hydrogel impregnated with bFGF (bFGF group) and the other was treated with gelatin hydrogel impregnated with saline (control group). Facial movement scoring, electrophysiological testing, and histological assessment of facial neurons were performed. The freezing-induced facial paralysis model showed a facial neuronal cell death rate of 29.0%; however, bFGF administration reduced neuronal cell death to 15.8%. Facial movement scores improved in the bFGF group compared with those in the control group. Intratympanic bFGF administration has a protective effect on facial neurons in a model of severe facial paralysis. These findings suggest a potential therapeutic approach for treating patients with refractory facial paralysis. Further studies are required to explore the clinical applicability of this treatment.
外周神经严重的轴突损伤会导致向中枢侧的逆行性变性,进而导致神经元细胞死亡,最终导致轴突再生不完全和功能恢复不佳。因此,有必要在面神经麻痹模型中评估面神经核,并研究治疗效果,以确定针对严重麻痹的治疗方案。因此,我们旨在研究严重面神经麻痹模型中面神经细胞减少的百分比,以及鼓室内注射碱性成纤维细胞生长因子(bFGF)抑制神经元细胞死亡的程度。通过冷冻面神经管在哈特利豚鼠中诱导建立严重面神经麻痹模型。将动物分为两组:一组用浸渍有bFGF的明胶水凝胶治疗(bFGF组),另一组用浸渍有生理盐水的明胶水凝胶治疗(对照组)。进行面部运动评分、电生理测试以及对面部神经元的组织学评估。冷冻诱导的面神经麻痹模型显示面神经神经元细胞死亡率为29.0%;然而,给予bFGF后神经元细胞死亡率降至15.8%。与对照组相比,bFGF组的面部运动评分有所改善。鼓室内注射bFGF对严重面神经麻痹模型中的面部神经元具有保护作用。这些发现提示了一种治疗难治性面神经麻痹患者的潜在治疗方法。需要进一步研究来探索这种治疗方法的临床适用性。