牛痘疫苗致炎兔皮提取物治疗三叉神经痛的作用机制研究

目的:观察牛痘疫苗致炎兔皮提取物(analgecine)对于三叉神经痛的效果及镇痛机制.方法:将大鼠制成单侧缩窄性三叉神经痛模型,在痛觉超敏期随机分为两组.牛痘疫苗致炎兔皮提取物组:腹腔内注入牛痘疫苗致炎兔皮提取物100u/kg;生理盐水组:腹腔内注入生理盐水10ml/kg.2周后,观察大鼠疼痛阚值(PT)变化及缩窄环区域神经组织的改变.结果:(1)术后2周,动物出现痛觉过敏,PT明显减低;牛痘疫苗致炎兔皮提取物组PT逐渐升高,与治疗前及生理盐水组相比存在显著差异性(P<0.01).(2)痛觉超敏期大量神经纤维肿胀变性、髓鞘脱失.2周后,生理盐水组髓鞘脱失明显,无髓纤维数目增多;牛痘疫苗致炎兔皮提取物组神经纤维肿胀消失,髓鞘板层结构致密,与正常结构类似.结论:动物实验表明,牛痘疫苗致炎兔皮提取物对于三叉神经痛的镇痛效果肯定,其作用机制部分是通过促进受损变性的神经纤维修复实现.

STUDY ON MECHANISM OF ANALGECINE FOR TREATMENT OF TRIGEMINAL NEU-RALGIA

Objective:To observe analgecine's analgesic effect and mechanism on treatment of trigeminal neuralgia,and understand the analgecine's effect on myelinolysis following chronic constriction injury. Methods:Following the appearance of allodynia,rats with loosely ligated unilateral trigeminal nerve were randomly allocated,analgecine group and saline group.The pain-related behaviours and histological chan- ges were observed.Results:(1)Allodynia to mechanical stimulation on the territory of ligated nerve was found on the 2nd week post-operation.the pain threshold obviously reduced.The analgecine's analgesic effect was observed gradually after administration,the pain threshold was significantly greater than that in saline group and pre-administered(P<0.01).(2)On the 2nd week post-operation,the fiber of tri- geminal nerve were obviously degeneratet.On the 2nd week post-administration,in saline group,the fiber of trigeminal nerve were edema and demyelination.In analgecine group,the demyelination of nerves were significantly recovered.Conclusion:The analgesic effect of analgecine for trigeminal neuralgia is realized by recovery of injured nerve.