中文摘要：

目的 观察电针对易卒中型肾性高血压大鼠（RHRSP）大脑中动脉闭塞（MCAO）后第1、7、14、28日脑梗死颈髓Rho-A表达的影响,探讨电针对脑梗死远隔损害的可能机理.方法 雄性SPF级SD大鼠行双肾双夹＊复制RHRSP,再用线栓法制作MCAO模型,用随机数字表法分为模型组、电针组、假电针组、假手术组与高血压组.电针组选百会和大椎穴治疗,用尼氏染色检测脊髓神经元数目,Western blot检测Rho-A表达.结果 MCAO术后第28日,电针组神经元数量减少明显低于模型组与假电针组（P＜0.05）,脑梗死组、电针组、假电针组Rho-A表达较高血压组、假手术组明显升高（P＜0.05）,电针组Rho-A表达较脑梗死组、假电针组明显降低（P＜0.05）.结论 脑梗死后颈髓Rho-A表达增高是ACI远隔损害的重要原因,电针对高血压大鼠脑梗死中枢神经损伤的保护作用可能与其下调中枢神经生长抑制因子Rho-A表达等机制密切相关.

英文摘要：

Objective： To observe the effect of electric acupuncture on the cervical cord Rho-A expression of cerebral infarction in Stroke-prone-Renovascular-Hypertension-Rats （RHRSP） with middle cerebra/artery oc- elusion（MCAO） in the first,seventh,fourteenth and twenty-eighth day,and investigate the possible mechanisms of electric acupuncture on diaphragma damage in acute cerebral infarction（ACI）. Methods： Male SPF SD rats were duplicated the RHRSP Mode] and MCAO models were built by stringing middle cerebral artery occlusion. The MCAO models were randomly divided into model group,elelectroacupuneture group,sham elelectroacupuncture group,sham operated group and hypertension group. ＂Baihui＂ and ＂Dazhui＂ acupoints were eleetroacupuneted in electric acupuncture group. Then the number of neurons was checked by Nissl staining and Rho-A expression was detected by Western blot method. Results： 28 days after MCAO,the neurons number of elelectroacupuncture group decreased obviously than that of model group and sham elelectroacupuneture group （P〈0.05）. Rho-A ex- pression of model group, elelectroacupuncture group, and sham elelectroacupuncture group are obviously increased more than that of sham operated group and hypertension group （P〈 0.05）.Rho-A expression of eleleetroacupunc- ture group decreased more than that of model group and sham elelectroacupuncture group （P 〈 0.05）. Conclu- sion： The increase of cervical cord Rho-A expression after cerebral infarction is an important factor which pre- vents from ACI diaphragma damage. Protective effect of elelectroacupuncture to CNS injury in hypertension-rats with cerebral infarction may closely relate to its mechanism of decreasing Rho-A expression.