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1. 湖北中医学院
2. 武汉军械士官学校
纸质出版日期:2006
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毛庆菊, 王汉兵, 陈邦国, 等. 电针对局灶性脑缺血再灌注大鼠外周血中可溶性细胞间粘附分子-1和内皮素-1的影响[J]. 针刺研究, 2006,(5):272-275.
MAO Qing-ju, WANG Han-bing, CHEN Bang-guo, et al. Effects of Electroacupuncture on Plasma sICAM and ET-1 Contents in Cerebral Ischemia Rats[J]. Acupuncture research, 2006, (5): 272-275.
目的:探讨电针对大脑中动脉缺血再灌注模型大鼠外周血中可溶性细胞间粘附分子-1(sICAM-1)、内皮素-1(ET-1)含量的影响。方法:SD大鼠40只
随机分为正常对照组、假手术组、模型组、电针组
采用大脑中动脉线栓法制备局灶性脑缺血再灌注模型
于缺血再灌注24 h后摘除眼球采血
分别应用酶联免疫吸附法、放射免疫法观察脑缺血再灌注及电针对大鼠外周血中sICAM-1、ET-1含量的影响。结果:脑缺血再灌注后大鼠外周血中sICAM-1、ET-1的含量增高(模型组与正常组、假手术组比较P<0.01);电针可降低大鼠外周血中sICAM-1、ET-1的含量(电针组与模型组比较P<0.05)。结论:早期针刺治疗对脑缺血损害有效防治作用是通过改善脑血管内皮细胞功能而实现的。
Objective: To investigate the effect of electroacupuncture(EA) on plasma soluble intercellular adhesion molecule(sICAM)-1 and endothelin(ET)-1 contents in cerebral ischemia-reperfusion(CI/R) rats for revealing the underlying mechanism of acupuncture in preventing CI/R induced vascular endothelium injury. Methods: A total of 40 SD rats were randomly divided into normal control(n=10)
sham-operation(n=10)
model(n=10)
and EA(n=10) groups.CI/R model was established by electrocoagulation of the right external carotid artery and occlusion of the middle cerebral artery(MCA) with a nylon thread(burned global end) for 30 min and reperfusion under anesthesia(10% chloral hydrate
300 mg/kg).EA(4/16 Hz
1-3 V) was applied to "Baihui"(GV 20) and "Shuigou"(GV 26) for 30 min
and once again 12 hours later.Twenty-four hrs after CI/R
blood sample was collected by excising the rat's eyeballs for assaying plasma sICAM-1 and ET-1 contents with enzyme linked immunosorbent assay(ELISA) and radioimmune methods respectively. Results: In comparison with control group
both sICAM-1 and ET-1 contents in model group increased significantly(P<0.01)
while in comparison with model group
these two indexes of EA group decreased significantly(P<0.05).No significant differences were found between control and sham-operation groups in these two indexes. Conclusion: EA intervention can effectively reduce CI/R induced vascular endothelia injury
which may contribute to its action in clinically improving cerebral ischemia.
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