腺苷脱氨酶介导电针百会穴对脑缺血再灌注损伤大鼠脑保护效应的研究

作者	单位	E-mail
王宏法,夏洪莲,秦金玲,郏丹赟
王均炉	温州医学院附属第一医院麻醉科（温州325000）	wangjunlu@yahoo.com.cn

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中文摘要:

目的观察电针百会穴预处理对大鼠大脑皮质腺苷及腺苷脱氨酶（ADA）浓度的影响以及对大脑中动脉阻塞（middle cerebral artery occlusion，MCAO）缺血再灌注（ischemia reperfusion，I/R）大鼠神经功能评分及脑梗死体积的影响，探讨电针百会穴预处理缓解大鼠脑I/R的机制。方法将54只雄性SD大鼠随机分为假电针组、电针组、对照组，每组18只，对照组麻醉后不给任何干预，电针组大鼠给予电针百会穴30 min，假电针组针刺后不予通电其他程序同电针组，检测电针后30、60、120 min大鼠大脑皮质ADA及腺苷浓度的变化；建立脑I/R模型，将48只雄性SD大鼠随机分成6组：模型组（A组）、电针组（B组）、电针+腺苷A1受体拮抗剂（8-cyclopentyl-1，3-dipropylxanthine，DPCPX）组（C组）、电针+二甲基亚砜（DMSO）组（D组），脱氧柯福霉素组（E组）、生理盐水组（F组），B、C、D组于造模前2 h给予电针30 min，C、D组在电针前30 min分别给予腹腔注射DPCPX（1 mg/ kg）、DMSO（1 mL /kg），E、F组于造模前30 min分别腹腔注射脱氧柯福霉素（500 μg/kg）、生理盐水（1 mL/kg），再灌注24 h后对大鼠进行神经功能评分并检测其脑梗死体积。结果与假电针组比较，对照组各时间点皮质区腺苷及ADA差异无统计学意义（P>0.05）。与对照组同期比较，电针组60 min时ADA浓度降低［（315.0±22.9 U/L），P<0.05］，于电针后120 min恢复正常水平；电针组120 min时腺苷浓度升高［（20.4±2.2 ）ng/ μL，P<0.05］。与模型组比较，B、D、E组神经功能评分降低（P<0.05），脑梗死体积明显减小（P<0.01）。其他各组的脑梗死体积和神经功能评分与模型组比较差异无统计学意义。结论电针百会穴对脑I/R损伤大鼠脑保护效应可能是通过降低大脑皮质ADA水平，提高腺苷含量，进一步激活腺苷A1受体而实现的。

英文摘要:

Objective To observe the electroacupuncture （EA） pretreatment at Baihui （GV20） on the concentration of adenosine deaminase （ADA） and adenosine， and to evaluate its effects on the neurologic function score and the infarction volume after middle cerebral artery occlusion （MCAO） ischemia/reperfusion （I/R）， thus exploring its mechanisms for relieving the ischemia/reperfusion injury. Methods Totally 54 male SD rats were randomly divided into 3 groups， the sham EA group， the EA group， and the control group， 18 in each group. Rats in the control group were not intervened after anesthesia. Rats in the EA group were needled at Baihui （GV20） for 30 min. Rats in the sham EA group received the same procedure as those performed in the EA group without electricity connected. The changes of adenosine and ADA contents were detected at 30， 60， and 120 min after EA respectively. The I/R model was established. Totally 48 male SD rats were randomly divided into 6 groups， i.e.， the model group （Group A）， the EA group （Group B）， the EA+8 Cyclopentyl 1，3 dipropylxanthine （DPCPX） group （Group C）， the EA+DMSO group （Group D）， the Deoxycoformycin （Deo） group （Group E）， and the normal saline group （Group F）. Rats in Group B， C， and D received EA for 30 min before modeling. Rats in Group C and D were peritoneally injected with DPCPX （1 mg/ kg） and DMSO （1 mL/kg） at 30 min before EA. The neurologic function score was evaluated and the infarct volumes were detected after 24 h reperfusion. Results Compared with the sham EA group， there was no statistical difference in the contents of the adenosine or ADA in the control group at each time point （P>0.05）. Compared with the control group at the same time point， the content of ADA significantly decreased at 60 min in the EA group ［（315.0±22.9 U/L）， P<0.05］， and restored to the normal level at 120 min after EA. The content of adenosine increased in the EA group at 120 min ［（20.4±2.2） ng/ μL， P<0.05］. Compared with the model group， the neurologic function score decreased （P<0.05） and the infarct volumes were obviously reduced （P<0.01） in Group B， D and E. There was no statistical difference in the neurologic function score or the infarct volumes in other groups， when compared with the model group （P>0.05） Conclusion EA at Baihui （GV20） showed protective effects on the cerebral I/R rats， which might be achieved through lowering the ADA concentration and elevating the adenosine content， and further activating adenosine A1 receptor.

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