电针预处理对全脑缺血再灌流大鼠炎性细胞因子的影响

目的研究炎性细胞因子在急性全脑缺血再灌流损伤中的作用及电针预处理的保护作用机理。方法SD大鼠随机分为假手术组、模型组、电针治疗组（左侧肩隅、外关、髀关、足三里）、穴位对照组（左侧清灵渊、灵道、萁门、漏谷穴）、非穴位对照组（左侧天泉与曲泽连线中点、曲泽与郗门中点、五里与阴胞连线中点和膝关与中都连线中点）。三动脉结扎法造成大鼠全脑缺血再灌注损伤模型，放射免疫法测定血浆内皮素（ET）、白介素-1β（IL-1β）、白介素-6（IL-6）和肿瘤坏死因子（TNF-α）含量。结果与假手术组比较，模型组结扎颈总动脉30min的血浆IL-1β含量显著升高（P〈0．05），血浆IL-6和TNF-α含量均有升高的趋势，但无显著性差异（P〉0．05）；再灌注30min，血浆IL-1β和TNF-α含量均显著升高（P〈0．05），血浆IL-6有升高的趋势，但无显著性差异（P〉0．05）。循经取穴电针能显著降低大鼠脑缺血和再灌注血浆IL-1β、IL-6和TNF-α含量，与模型组、穴位对照组或非穴位对照组比较差异有统计学意义。结论脑缺血再灌注急性期可导致血浆IL-1β、IL-6和TNF-α含量升高，电针治疗脑缺血再灌注损伤的机制之一与降低炎性细胞因子含量及阻断炎症级联反应有关。

Effect of electroacupuncture on inflammatory factors in blood of rat with cerebral Ischemia reperfusion

Objective To observe the change of IL-1β,IL-6 and TNF-α content after cerebral ischemia/reperfusion（CL/R） and the effect of electroacupuncture-（EA）. Methods 55 SD rats were evenly randomized into sham-operation,-model, EA, acupoint-control and non-acupoint control groups. CI/R model was produced by occlusion of the basilar artery and bilateral common carotid arteries and reperfusion. Carotid venous blood was collected 30 rain after CI and after CI/R respectively for analyzing plasma IL-1β ,IL-6 and TNF-α content with radioimmunoassay. Results Compared with sham-operation group, plasma IL-1β contents of model group 30 min after CI and CI/R and plasma TNF-α contents of model group 30 min after CI/R increased significantly（ P 〈0. 05）. While compared with model group,plasma IL-1β contents of EA group 30 min after CI/R,plasma IL- 6 contents of EA group 30 min after CI and CI/R decreased significantly（ P 〈 0. 05 - P 〈 0. 001 ）. Plasma IL-1β and IL-6 levels of acupoint-control and non-acupoint control groups 30 min after CI or CI/R and plasma TNF-α level of non-acupoint control groups 30 min after CI/R were markedly higher than that of EA group at the same time course. Conclusion Plasma IL-1β,IL-6 and TNF-α content increases at the early period after ischemic brain injury. The therapeutic action of EA on cerebral isehemia reperfusion can be realized by decrease plasma IL-1β,IL-6 and TNF-α content and inflammatory response induced by eytokines.