摘要
目的探讨电刺激对脊髓损伤后神经胶质纤维酸性蛋白(GFAP)、白细胞介素-1α(IL-1α)表达的影响。方法健康成年SD大鼠72只随机分为正常组、损伤组、电刺激组。采用Allen's法将后两组复制为脊髓T9损伤模型。术后对电刺激组大鼠进行电刺激治疗7 d。3组均进行BBB评分,免疫组织化学检测GFAP与IL-1α的表达情况。结果损伤组和电刺激组BBB评分均小于正常组(P<0.05),伤后5 d、7 d,电刺激组较损伤组BBB评分增加(P<0.05)。损伤组、电刺激组GFAP阳性表达均在伤后5 d达到高峰,伤后5 d、7 d,电刺激组GFAP表达低于损伤组(P<0.05);IL-1α阳性表达在伤后7 d内持续上升,伤后5 d、7 d,电刺激组IL-1α表达低于损伤组(P<0.05)。结论电刺激能抑制GFAP与IL-1α的表达,可能有利于减轻炎症反应,减少胶质瘢痕形成。
Objective To investigate the effects of electrical stimulation on the expression of glial fibrillary acidic protein(GFAP) and interleukin-1 alpha(IL-1α) in adult rats with spinal cord injury.Methods 72 adult SD rats were randomly divided into damage group(n= 24),electrical stimulation group(n=24) and normal group(n=24).The spinal cord incomplete injury model on T 9 was made with Allen's method in the former 2 groups.The rats in electrical stimulation group accepted electrical stimulation for 7 d.All the rats were evaluated with the Basso,Beattie Bresnahan locomotor rating scale(BBB scale),and the expression of GFAP and IL-1α were determined with im-munohistochemistry.Results The BBB scores in both the damage group and electrical stimulation group were significantly less than that in the normal group(P0.05),and it was more in the electrical stimulation group than in the damage group 5 and 7 d after injury.The expres-sions of the GFAP significantly increased after injury to the peak on 5th day,while it was less in the electrical stimulation group than in the damage group 5 and 7 d after injury(P0.05).The expressions of the IL-1α increased continually after injury,while it was less in the electri-cal stimulation group than in the damage group 5 and 7 d after injury(P0.05).Conclusion Electrical stimulation can inhibit the expression of GFAP and IL-1α,that reduce inflammation and glial scar formation.
出处
《中国康复理论与实践》
CSCD
2011年第9期844-847,共4页
Chinese Journal of Rehabilitation Theory and Practice
基金
四川省科技厅课题(2008SZ0053)
成都医学院创新实验项目(CX2010035)
关键词
脊髓损伤
电刺激
神经胶质纤维酸性蛋白
白细胞介素-1Α
spinal cord injury
electrical stimulation
glial fibrillary acidic protein
interleukin-1 alpha