电针对急性脑梗死大鼠皮层神经蛋白聚糖表达的影响  

Effect of electro-acupuncture on neurocan expression in the peri-infarct cortex in rats with acute cerebral infarction

作　　者：张爱武[1] 方燕南[1] 王雪晶[1] 姜涛[2] 

机构地区：[1]中山大学附属第一医院神经科,广州510080 [2]南方医科大学华瑞医院神经内科,广州510630

出　　处：《中华神经医学杂志》2009年第2期140-144,共5页Chinese Journal of Neuromedicine

摘　　要：目的探讨电针治疗对脑梗死后不同时间点神经蛋白聚糖（neurocan）表达的影响。方法将90只SD大鼠采用随机数字表分为假手术组、大脑中动脉闭；N（MCAO）模型组、电针治疗组。用电凝法建立MCAO模型，选取内关、外关、足三里、三阴交四穴给予电针刺激，连续治疗4周。选取1、2、4周三个时间点用免疫荧光检测neurocan蛋白的分布，应用实时荧光定量RT．PCR、Westernb lot方法检测neurocanmRNA、neurocan蛋白的表达情况。结果neurocan主要分布于梗死灶周围区域的胶质细胞及细胞间隙。MCAO模型组neurocan mRNA表达在梗死后1周明显增高。且梗死后2周（0．806±0．224）表达达峰值，持续至梗死后4周仍表达仍增多；电针治疗组neurocan mRNA表达在电针治疗后1周明显降低，而后逐渐下降，至4周（0．031±0．018）达最低值。MCAO模型组neurocan蛋白表达明履增高，且有逐渐升高趋势，术后4周（0．878±0．049）达最高值；电针治疗组neurocan蛋白表达在电针治疗后2周明显降低，而后逐渐下降，至4周（0．292±0．042）达最低。以上差异均有统计学意义（P均〈0．05）。结论电针对脑梗死后neurocan的表达增加起抑制作用，这可能是电针抑制胶质瘢痕形成的机制之一。Objective To investigate the effect of electro-acupuncture （EA） on neurocan expression in the peri-infarct cortex in rats after middle cerebral artery occlusion （MCAO）. Methods Ninety SD rats were randomly divided into sham-operated group （SO）, MCAO group and EA treatment group （ET）. Heat-coagulation method was used to establish MCAO in the rats in the latter two groups. The rats in the ET group received EA treatment at the acupoints Neiguan, Waiguan, Zusanli and Sanyinjiao for 1, 2, 3, or 4 weeks after MCAO. Immunohistochemistry, quantitative real-time RT-PCR and Western blotting were used to detect the expression of neurocan in the peri-infarct cortex after the treatment. Results Neurocan expression was detected in and around the GFAP-positive cells near the cerebral infarct loci following MCAO. Neurocan mRNA in rats with MCAO increased significantly 1 week after MCAO, reaching the peak level （0.806±0.224） in the second week and maintained the high expression level till 4 weeks after MCAO. In the EA treatment group, neurocan mRNA began to decrease in the first week of EA treatment followed by gradual decrease till reaching the lowest level （0.031 ±0.018） in the 4th week of EA treatment. In the rats in MCAO group, the expression of neurocan protein increased progressively 1 week after MCAO and reached the highest level in the fourth week （0.878± 0.049）; EA treatment significantly reduced neurocan expression in the second week of treatment, and resulted in the lowest expression level （0.292 ±0.042） in the fourth week of treatment. All these differences were statistically significant （P〈0.05）. Conclusions EA treatment can inhibit the expression ofneurocan in the peri-infarct area, which might be one of the mechanisms of EA to reduce glial scar formation after cerebral infarction.

关 键 词：电针 神经蛋白聚糖 脑梗死 

分 类 号：R686[医药卫生—骨科学]