摘要
目的:探索电针对脑缺血再灌注大鼠大脑受损神经元的保护作用及其钙调蛋白信号转导机制。方法:随机将25只SD大鼠均分为假手术组、模型组、电针组、TFP组和电针+TFP组。采用改良Longa线栓法制作局灶性大脑中动脉缺血再灌注模型。电针组取"百会""大椎"穴,选用疏密波,持续电刺激30 min。TFP组腰穿缓慢注入钙调蛋白阻滞剂三氟拉嗪(TFP)40μL/kg。电针+TFP组腰穿注射TFP并电针,其用药方法及取穴均同TFP组和电针组。假手术组和模型组不予治疗干预。依据Julio氏神经行为学评分法对各组大鼠进行评分,采用免疫组织化学染色法观察不同干预下模型大鼠海马钙调蛋白(CaM)的表达。结果:①神经行为学评分:与模型组(6.90±1.66)相比,电针组(14.50±1.08)、TFP组(11.70±1.06)、电针+TFP组(14.30±1.06)均显著升高(均P<0.01),但仍低于假手术组(17.60±0.52)(均P<0.01);其中电针组又优于TFP组(P<0.01)。②大鼠海马CaM的蛋白免疫阳性表达评分:与假手术组(0.080±0.045)相比,模型组(1.680±0.268)显著升高(P<0.01);与模型组(1.680±0.268)相比,电针组(0.880±0.179)、TFP组(0.720±0.179)和电针+TFP组(0.420±0.249)均明显下调(均P<0.01);其中电针+TFP组又明显低于TFP组(P<0.05)。结论:电针可减轻脑缺血再灌注大鼠大脑神经元的损伤,促进损伤修复,这一作用可能与其影响缺血再灌注后钙调蛋白信号有关。
Objective To investigate the protective effect of electroacupuncture （EA） on injured neurons and the signal transduction mechanism of calmodulin （CAM） in rats with cerebral ischemia-reperfusion injury （CIRI）. Methods A total of 25 SD rats were randomly divided into a sham-operation group, a model group, an EA group, a TFP group and an EA＋TFP group. The rat model of middle cerebral artery occlusion （MCAO） was established by the modified Longa thread occlusion method. The EA group was treated with EA at ＂Dazhui＂ （GV 14） and ＂Baihui＂ （GV 20） for 30 minutes. The TFP group was treated with lumbar intrathecal injection of Trinuoperazine （TFP） at a dose of 40 μL/kg, the inhibitor of CaM. The EA＋TFP group was treated with EA combined with TFP, and the sham-operation group and the model group without any treatment. The neurology deficit score was evaluated by the Julio＇s neuroethology score methods in all rats, and the expression of CaM in cerebral hippocampus tissue was detected with immunohistochemical method in different intervention condition. Results OIn comparison with the model group of 6. 90 ±1.66, the neuroethology score in the EA group of 14.50±1.08, the TFP group of 11.70=t=1.06 and the EA ±TFP group of 14.30±1.06 were all significantly mcreased （all P〈：0.01）, while those still were all lower than the sham group of 17.60±0. 52 （all P〈0.01）, and the EA group was better than the TFP group （P〈0.01）. ②In comparison with the sham group of 0. 080± 0. 045, the immune positive expression score of CaM protein in hippocampus in the model group of 1. 680±0. 268 was significantly increased （P〈0.01）. In comparison with the model group,the expression score of CaM protein in the EA group of 0. 880±0. 179, the TFP group of 0. 720±0. 179 and the EA ＋TFP group of 0. 420~0. 249 were all significantly reduced（all P〈0.01）,and the expression score of CaM in the EA＋TFP group was lower than that in the TFP group（P〈0.05）,Conclusion EA can reduce the injury of cerebral neurons induced by CIRI in rats and promote the recovery,which may be related to its effect in rffect in regulating CaM signaling pathway after the ischemia reperfsion injury.
出处
《中国针灸》
CAS
CSCD
北大核心
2011年第11期1015-1019,共5页
Chinese Acupuncture & Moxibustion
基金
国家自然科学基金资助项目:30772836
关键词
脑卒中
脑缺血
电针
钙调蛋白
三氟拉嗪
Stroke Brain Ischemia Electroacupuncure
Calmodulin
Trinuoperazine
