远程缺血后适应对脑缺血损伤的实验研究

目的探讨远程缺血后适应对大鼠大脑中动脉缺血2h再灌注24h脑梗死体积、神经功能评分及Caspase-3表达的影响。方法大鼠脑缺血模型采用线栓法制备。缺血SD大鼠（280～300g）48只，随机分为假手术组（n=6）、对照组（即单纯脑缺血／再灌注损伤，n=14）和远程缺血后适应组（脑缺血后给予双下肢的非致死性的缺血再灌注）。根据后适应时间不同，后组者又分为缺血即刻后适应组（n=14）和再灌注即刻后适应组（n=14）。于大脑中动脉再灌注24h进行神经功能评分、脑组织梗死体积以及Caspase-3表达的测定。脑组织梗死体积采用四氮唑红（TTC）染色法测定。Caspase-3的表达应用免疫组织化学法检测。结果远程缺血后适应组的脑梗死体积与单纯缺血组相比明显降低，差异有显著性（P〈0．05）；与假手术组相比，单纯缺血组Caspase-3阳性细胞数明显增多，差异有显著性（P〈0．05）；与对照组比较，缺血即刻后适应组Caspase-3阳性细胞数降低，差异有显著性（P〈0．05）。结论远程缺血后适应能减轻脑缺血／再灌注损伤，其保护作用可能与降低Caspase-3的表达有关。

Experimental study of remote ischemic post - conditioning on cerebral ischemia in rats

Objective To study the effects of remote ischemic post - conditioning on the infarct volume, neurological functional scores and expression of Caspase -3 in rat brain following 2 h middle cerebral artery occlusion and 24 h reperfusion. Methods 48 SD rats, weighing 280 - 300 g, were randomly assigned into four groups ： sham group （ n = 6 ）, control （ cerebral ischemia/reperfusion） group （ n = 14） , and remote post - conditioning group, including post - conditioning at beginning of ischemia group （ n = 14 ） and post - conditioning at beginning of reperfusion group （ n = 14 ）. The infarct volume and neurological behavior test were determined in control, post - conditioning at beginning of ischemia, and post - conditioning at beginning of reperfusion groups at 24 h after reperfusion. The expression of Caspase - 3 was determined in sham, control, post - conditioning at beginning of ischemia groups at 24 h after repeffusion by immunohistochemistry. Results The per- centage of infarct volume was significantly lower in the remote ischemic post - conditioning groups compare to the control group （P 〈 0. 05 ）. The expression of caspass - 3 was increased in the control group comared to the sham group （ P 〈 0. 05 ）. Caspase - 3 expression was decreased in the post - conditioning at beginning of ischemia group compared with the control group （ P 〈 0. 05 ）. Conclusion Remote ischemic post - conditioning has a neuroprotective effects on the cerebral ischemia in rats. One of the mechanisms of neuroprotections by remote ischemic post - conditioning may be due to the decrease of Caspase - 3 expression.