摘要
目的:观察急性脑缺血再灌注大鼠脑梗死体积和脑内白细胞介素1β蛋白表达的变化情况,探讨电针干预急性脑缺血病理过程的作用途径。方法:实验于2005-05/08在河南中医学院实验中心完成。①分组:SD大鼠55只,采用随机数字表法随机分为假手术组5只,电针组25只,模型组25只。②模型制备:电针组和模型组参照Koizumi等建立的方法制备模型,经颈外动脉插入尼龙线,阻塞颈内动脉颅内段到达大脑中动脉分支处的起始部,引起大脑中动脉供血区的急性脑缺血,假手术组尼龙线不插到大脑中动脉起始部位,插入深度约12mm左右,其余步骤同模型组。③针刺方法:电针组造模后常规剪毛消毒用0.35mm×40mm毫针快速刺入皮下向左前下方(相当于人体曲鬓穴处)平刺,进针深度约0.8cm,另于风府穴直刺一针,深度约0.5cm。于缺血后10min给予电针,连接全能脉冲电疗仪,百会接阳极,风府接阴极,电针频率7Hz,强度6mA,30min/次。模型组造模后不进行任何处理。④缺血再灌注24h后电针组和对照组分别取5只大鼠用TTC染色法测定脑梗死体积。⑤电针组和模型组分为缺血再灌注2,6,12,24h4个观测时间点,每个时间点5只大鼠。应用免疫组化方法观察各组大鼠白细胞介素1β蛋白表达的变化。结果:55只大鼠均进入结果分析。①大鼠缺血2h再灌注24h后,模型组脑梗死体积大于电针组梗死体积[(137.76±19.90),(84.46±22.30)mm3,P<0.05]。②假手术组大鼠白细胞介素1β在皮质、纹状体呈基础水平表达,模型组和电针组脑缺血再灌注后2h白细胞介素1β表达开始增强,于再灌注后12h达高峰,但电针组再灌注后2,6,12,24h白细胞介素1β表达均较模型组弱(皮质:0.17±0.01,0.21±0.01;0.20±0.02,0.25±0.01;0.27±0.02,0.32±0.02;0.26±0.01,0.28±0.01,P均<0.05～0.01;纹状体:0.18±0.20,0.24±0.02;0.22±0.02,0.27±0.02;0.35±0.01,0.37±0.01;0.31±0.01;0.34±0.01,P均<0.05～0.01)。结论:电针可明显抑制皮质及纹状体白细胞介素1β蛋白的表达,同时缩小梗死的体积,说明电针对缺血性脑损伤的保护效应可能与其抑制脑内白细胞介素1β蛋白的表达有关。
AIM： To observe the changes in cerebral infarction volume in rats with acute cerebral ischemic reperfusion and the expression of cerebral interleukin 1β （IL 1β） protein, and explore the effecting pathway of electroacupuncture in the prevention of acute cerebral ischemic reperfusion.
METHODS： The experiment was conducted in the R＆D Center of Henan University of Traditional Chinese Medicine from May to August 2005. （1） Grouping： Fifty-five SD rats were randomly divided into the sham-operation group （n=5）, electroacupuncture group （EA group, n=25） and model group （n=25）. （2） Model establishment： Rats in the EA group and model group were established into models according to Koizumi method： The nylon strain was inserted via the external carotid artery （ECA） to prevent the intraeal parts of internal carotid （IC） from reaching to the beginning in the branch of cerebral artery, so as to prevent the acute cerebral ischemia in the blood-supply region of middle cerebral artery （MCA）. While the nylon strain was inserted into the brain of rats in the sham-operation group for about 12 mm without reaching to the beginning of MCA, while the rest procedures were the same to those in the model group. （3） Acupuncture methods： Rats in the EA group were sheared off the hairs after modeling to rapidly prick subcutaneously to the left anterior direction （the Tortuous Sideburns acupoint in buman body） with a 0.35 mm×40 mm acupuncture needle with the depth of needling of about 0.8 cm. Meanwhile, the acupoint of Fengfu was directly needled at the depth of over 0.5 cm, and the EA was performed at 10 minutes after ischemia by connecting with all round pulse electro-therapeutic apparatus, and Baihui was connected with the positive polar, while the Fengfu was connected with the negative polar at the frequency of 7 Hz and the intensity of 6 mA with 30 minutes for each time. Rats in the model group received no treatment after the modeling. （4） Twenty-four hours after the ischemic reperfusion, 5 rats were selected from the EA group and control group for TTC stainning to determine the volume of cerebral infarction. （5） Rats in the EA group and modeling group were re-divided into 4 groups according to the time： 2 hours, 6 hours, 12 hours and 24 hours post-isehemic reperfusion groups with 5 rats in each time-point. The changes in IL 1β protein expression were detected by immunohistochemical method in each group.
RESULTS： All 55 rats were involved in the analysis of results （1） At 24 hours after reperfusion following 2-hour ischemia, the volume of cerebral infarction was larger in tbc model group than that in the EA group [（137.76±19.90） ,（84.16±22.30） mm^3,P 〈 0.05]. （2） Cerebral IL1β protein expressions of cortex and corpus striatum in sham-operation group were in basic level, while those in the model group and EA group were increased at 2 hours after cerebral ischemic reperfusion, which peaked at 12 hours after reperfusion, while the IL1β protein expressions in the EA group at 2 hours, 6 hours, 12 hours and 24 hours after reperfusion were weaker than those in the model group （Cortex： 0.17±0.01, 0.21±0.01, 0.20±0.02, 0.25±0.01, 0.27±0.02, 0.32±0.02, 0.26±0.01, 0.28±0.01, P 〈 0.05-0.01; Corpus striatum： 0.18±0.20, 0.24±0.02; 0.22±0.02, 0.27±0.02; 0.35±0.01, 0.37±0.01; 0.31±0.01, 0.34±0.01, P 〈 0.05-0.01）.
CONCLUSION： EA can markedly restrain the expression of cerebral IL1β protein in cortex and corpus striatum and decrease the volume of cerebral infarction. It suggests that the protection of EA on isehemic cerebral injury may be related with its inhibition on the expression of cerebral IL β protein.
出处
《中国临床康复》
CSCD
北大核心
2006年第43期153-155,共3页
Chinese Journal of Clinical Rehabilitation
作者简介
张振强★，男，1972年生，汉族，河南医科大学毕业，硕士，讲师，主治医师，主要从事内科脑病的实验和临床研究。
