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

STUDY ON MECHANISM OF ANALGECINE FOR TREATMENT OF TRIGEMINAL NEURALGIA

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10m l/kg。2周后,观察大鼠疼痛阈值(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。

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 changes 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 preadministered （P 〈 0.01 ）. （2） On the 2nd week postoperation, 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.