地佐辛减轻CCI大鼠神经病理性疼痛的实验研究

Experimental Study of Dezocine Inhibits the Neuropathic Pathologic Pain in CCI Rats

目的通过建立坐骨神经慢性压迫性疼痛(Chronic constriction injury,CCI)模型大鼠,观察腹腔注射地佐辛的镇痛作用及其可能机制。方法 SD大鼠32只,随机分为假手术(Sham)组、模型(Model)组、地佐辛2.5mg·kg^(-1)(D1)组和地佐辛10mg·kg^(-1)(D2)组等4组,每组8只,各组于手术后即刻至术后7天,每天腹腔注射1次药物,假手术组和模型组给予等体积的生理盐水。造模前和造模后1、3、5、7d观察各组大鼠的机械痛阈变化,于造模后7d免疫荧光组织化学法观测各组脊髓胶质纤维酸性蛋白(Glial Fibrillary Acidic Protein,GFAP)表达。结果大鼠建模1天后,PWT显示CCI大鼠的机械痛阈均出现明显下降,模型组在3d时降到最低,地佐辛干预的D1组在3d对CCI大鼠的痛阈有所改善(P<0.05),随后改变不大,D2组对大鼠的痛阈有明显改善,在5d时提高最为明显(P<0.01),同时,可见7d时各组脊髓GFAP的表达有所区别,模型组GFAP的表达明显增强,D1组较模型组表达减弱(P<0.05),D2组较模型组差异有显著的统计学意义(P<0.01)。结论地佐辛对神经病理性疼痛的抑制作用可能与下调脊髓GFAP的表达,影响星形胶质细胞的活化有密切关联。

OBJECTIVE Through the establishment of chronic sciatic nerve compression pain （chronic con- striction injury, CCI） rat model, to observe the analgesic effect of intraperitoneal injection of dezocine and its possible mechanism. METHODS Thirty two SD rats randomly divided into sham-operation group, model group, D1 group （with 2. 5mg · kg- 1 dezocine）, and D2 group （with 10mg · kg-1 dezocine）. Eight SD rats in each group. The SD rats in dezocine group were treated with dezocine by intraperitoneal injection once every day from the beginning to seven days after operation;but the SD rats in sham-operation group and model group were treated with isochoric normal sa- line. the changes of pain threshold of rats in the each group was detected at the time of 1,3,5,7 days before modeling and 1,3,5,7 days after modeling. 7 days after modeling, detected the expression of Glial Fibrillary Acidic Protein in the four groups by immunofluorescence histochemistry. RESULTS After 1 day of modeling, PWT showed a signifi- cant decrease in mechanical pain threshold in CC! rats,the model group decreased to a minimum at 3d,and the pain threshold was significantly improved in D1 group of dezocine（ P 〈 0. 05 ） ,followed by little change. D2 group signifi- cantly improved the pain threshold in rats,the most significant increase at 5d （P 〈0. 01 ）. At the same time,the ex- pression of GFAP in spinal cord of each group was different at 7d, the expression of GFAP in model group was signifi- candy enhanced, and the expression in D1 group was weaker than that of model group （ P 〈 0. 05 ）. There was signifi- cant difference between D2 group and model group （P 〈 0. 01 ）. CONCLUSION Dezocine can inhibit the neuro-pathic pathologic pain. The mechanism of it may relate to the decrease of the expression of GFAP in spinal cord andinfluence the activation of astrocytes.