摘要
目的电针督脉对大鼠脊髓损伤后水通道蛋白4(AQP4)表达和后肢功能恢复的影响。方法取SD大鼠150只,分为正常组(50只)、模型组(50只)、电针组(50只),模型组和电针组用改良的Allen法制成脊髓损伤模型,于模型成功后,电针组针刺督脉上大椎和命门穴3min,每天1次,连续7天。于实验第1、3、7、14、21天分别对大鼠后肢功能进行BBB评分,应用免疫组织化学技术检测脊髓组织AQP4的表达,用图像分析仪进行定量分析。结果脊髓损伤后第1天,模型组和电针组受损脊髓灰质、白质中AQP4的表达明显增加;第3天时均达到高峰,但电针组低于模型组(P<0.05)。第7、14、21天,与模型组比较,电针组AQP4表达也较低(P<0.01)。结论电针督脉使脊髓损伤后AQP4表达减少,这可能有利于抑制脊髓水肿、消除脊髓继发性损伤,保存了残存正常脊髓组织并促进神经组织重建。
ObjectiveTo investigate effects of electro-acupuncture (EA) on Du Meridian on the water channel aquaporin-4 (AQP-4) expression and hind limbs function recovery in experimental spinal cord injured rats. MethodsOne hundred and fifty SD rats were divided into the normal group, the model group and the EA group, with 50 rats in each group, modified Allen method was used to establish spinal cord injury model in the model and EA group. Rats in the EA group was EA on Dazhui and Ming men acupoints after modelling successfully. At the 1st, 3rd, 7th, 14th and 21th day after injury, the hind limbs function of rats was evaluated by BBB scales respectively, and the AQP-4 expression in spinal cord tissue was determined by immunohistochemistry technique and quantity analysed with image analyzer. ResultsAt the 1st day after spinal cord injury, the AQP-4 expression was significantly increased in gray matter and white matter of spinal cord in the model group and the EA group, which reached the peak at the 3rd day, but showed significant difference between the two groups (P<0.05), and the difference at the 7th, 14th and 21th day became more significant (P<0.01). ConclusionEA on Du Meridian can down-regulate AQP-4 expression after spinal cord injury, inhibit spinal cord edema for alleviating secondary spinal cord lesion, so as to protect the residual normal spinal cord tissues and promote the rebuilding of nervous tissues.
出处
《中国中西医结合杂志》
CAS
CSCD
北大核心
2005年第7期637-639,共3页
Chinese Journal of Integrated Traditional and Western Medicine
基金
国家自然科学基金资助项目(No.30371837)
关键词
电针
督脉
实验性脊髓损伤
水通道蛋白-4
electro-acupuncture
Du Meridan
experimental spinal cord injury
water channel aquaporin-4
