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目的探讨非侵入性远端肢体缺血后处理对大鼠脑缺血-再灌注损伤的神经保护作用。方法 SD大鼠45只随机均分为三组。A组大脑中动脉阻塞脑缺血90min后,行再灌注。B组于再灌注即刻行远端肢体缺血后处理:缺血5min,再灌注5min,循环4次。C组为假手术对照。脑缺血-再灌注后24h行神经功能缺损评分,检测相关指标。结果 B组神经功能缺损评分、脑梗死体积、脑组织含水量、半影区神经细胞凋亡数和Bax蛋白阳性细胞数均低于A组(P<0.05)。B组Bcl-2蛋白阳性细胞数及Bcl-2/Bax比值高于A组(P<0.05)。结论非侵入性远端肢体缺血后处理对大鼠脑缺血-再灌注损伤具有保护作用;其机制可能与调控Bcl-2和Bax蛋白表达和减少神经细胞凋亡有关。
Objective To investigate the neuroprotective effect of noninvasive distal limb ischemic postconditioning on cerebral ischemia-reperfusion injury in rats. Methods 45 SD rats were randomly divided into three groups. A group of middle cerebral artery occlusion cerebral ischemia 90min, reperfusion. In group B, distal limb ischemic postconditioning was performed immediately after reperfusion: ischemia for 5 min, reperfusion for 5 min and recycle for 4 times. Group C sham control. Neurological deficit scores were measured 24h after cerebral ischemia - reperfusion to detect the related indexes. Results The score of neurological deficit, the volume of cerebral infarction, the water content of brain tissue, the number of neuronal apoptosis in penumbra and the number of Bax positive cells in group B were lower than those in group A (P <0.05). The number of Bcl-2 positive cells and the ratio of Bcl-2 / Bax in group B were higher than those in group A (P <0.05). CONCLUSION: Noninvasive distal limb ischemic postconditioning has a protective effect on cerebral ischemia-reperfusion injury in rats. The mechanism may be related to the regulation of Bcl-2 and Bax protein expression and the reduction of neuronal apoptosis.