尼莫地平对大鼠面神经损伤的保护作用及GDNF表达的影响

目的 探讨尼莫地平对大鼠面神经损伤的保护作用及对胶质细胞源性神经生长因子(GDNF)表达的影响.方法 96只大鼠按随机数字表法分为假手术组、单纯损伤组、尼莫地平预处理组、尼莫地平后处理组,后三组建立大鼠面神经电损伤模型.应用HE染色、Western blotting等方法,观察大鼠面神经损伤后不同时期(1、3、6月)GDNF的动态表达变化及尼莫地平不同给药时间对其表达的影响.结果 与单纯损伤组相比,尼莫地平预处理组大鼠面神经损伤程度减轻,GDNF表达升高,持续时间延长;尼莫地平预处理组GDNF表达和尼莫地平后处理组间比较差异有统计学意义(P＜0.05);尼莫地平后处理组GDNF表达在3月、6月时与单纯损伤组比较差异无统计学意义(P＞0.05).结论 预防性应用尼莫地平可以保护面神经,其机制可能是通过调节GDNF的表达而实现的.

Abstract：

Objective To study the protective function of nimodipine on facial nerve injury and its effect on the expression of glial cell line-derived neurotrophic factor (GDNF). Methods Ninety-six SD rats were randomly divided into sham-operated group, facial nerve injury group, nimodipine pretreatment group, and nimodipine post-treatment group. Rat models of facial nerve injury in thc later 3groups were established. The dynamic changes of expression of GDNF were observed by HE staining and Western blotting in different treatment groups and at different time points (1, 3 and 6 months after the injury). Restdts Compared with the facial nerve injury group, the nimodipine pretreatment and post-treatment groups had significantly less severe nerve damage and significantly up-rcgulated expression of GDNF (P＜0.05). The expression of GDNF in the nimodipine pretreatment group was statistically higher than that in the nimodipine post-treatment group (P＜0.05). However, the expression of GDNF in the nimodipine post-treatment group was not statistically different from that in the facial nerve injury group 3 and 6 months after the injury (P＞0.05). Conclusion Nimodipine has significant facial nerve protective effect, and one of the mechanisms of nimodipine to protect the facial nerve is to regulate the GDNF expression.

Protective function of nimodipine on facial nerve injury and its effect on expression of glial cell line-derived neurotrophic factor

Objective To study the protective function of nimodipine on facial nerve injury and its effect on the expression of glial cell line-derived neurotrophic factor (GDNF). Methods Ninety-six SD rats were randomly divided into sham-operated group, facial nerve injury group, nimodipine pretreatment group, and nimodipine post-treatment group. Rat models of facial nerve injury in thc later 3groups were established. The dynamic changes of expression of GDNF were observed by HE staining and Western blotting in different treatment groups and at different time points (1, 3 and 6 months after the injury). Restdts Compared with the facial nerve injury group, the nimodipine pretreatment and post-treatment groups had significantly less severe nerve damage and significantly up-rcgulated expression of GDNF (P＜0.05). The expression of GDNF in the nimodipine pretreatment group was statistically higher than that in the nimodipine post-treatment group (P＜0.05). However, the expression of GDNF in the nimodipine post-treatment group was not statistically different from that in the facial nerve injury group 3 and 6 months after the injury (P＞0.05). Conclusion Nimodipine has significant facial nerve protective effect, and one of the mechanisms of nimodipine to protect the facial nerve is to regulate the GDNF expression.