Effect of electro-acupuncture on neurocan expression in the peri-infarct cortex in rats with acute cerebral infarction
10.3760/cma.j.issn.1671-8925.2009.02.009
- VernacularTitle:电针对急性脑梗死大鼠皮层神经蛋白聚糖表达的影响
- Author:
Ai-Wu ZHANG
1
;
Yan-Nan FANG
;
Xue-Jing WANG
;
Tao JIANG
Author Information
1. 中山大学附属第一医院
- Keywords:
Electro-acupuncture;
Neuroean;
Cerebral infarction
- From:
Chinese Journal of Neuromedicine
2009;8(2):140-144
- CountryChina
- Language:Chinese
-
Abstract:
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 foci 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 of neurocan in the peri-infarct area, which might be one of the mechanisms of EA to reduce glial scar formation after cerebral infarction.
