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目的：探讨大鼠缺血预适应在中低温低流量（MHLF）神经保护中的作用机理。方法60只雄性SD大鼠随机均分为三组：手术组在中低温下夹闭颈总动脉2 h后重新开放，模拟M H L F过程；假手术组不夹闭颈总动脉；缺血预适应组先夹闭双侧颈总动脉2 min ，然后开放5 min ，重复4次后再与手术组相同操作。采用免疫组化、RT-PCR和Western blot检测各组大鼠脑细胞在不同时间点的凋亡水平及线粒体凋亡信号通路各节点蛋白表达的变化。结果与手术组相比，缺血预适应组在不同时间点的细胞凋亡水平、细胞色素C和Caspase-3的活性下降，线粒体凋亡信号通路中Bcl-2蛋白表达增强，Bax蛋白表达减弱（ P＜0．05或P＜0．01）。结论 M H L F过程中，缺血预适应通过抑制线粒体凋亡信号通路发挥了神经保护作用。“,”Objective To investigate the molecular mechanism of ischemic preconditioning in neuroprotection during moderate hypothermic low flow (M HLF) procedures in rats .Methods Sixty male SD rats were randomly and equally divided into three groups .The rats without clamping common carotid artery in group C were taken as the blank control .Bilateral common carotid arteries of rats in group A were occluded for 2 hours at (25.0 ± 0.5)℃ of body temperature and then reopened and rewarmed .Bilateral common carotid arteries of rats in group B were occluded for 2 minutes and reopened for 5 minutes ,which was repeated for 4 times before conducting the process as in group A . The apoptosis of brain cells and the target proteins in mitochondrial apoptotic signaling pathway were measured at different time points by immunohistochemistry ,RT-PCR and Western blot .Results Compared with group A ,the apoptosis ,activities of cytochrome C and Caspase-3 at different time points were decreased ,Bcl-2 expression in mitochondrial apoptotic signaling pathway was enhanced , and Bax expression was weakened in group B ( P<0 .05 or P<0 .01 ) .Conclusion Ischemic preconditioning plays an important role in neuroprotection through suppressing the mitochondrial apoptotic signaling pathway during M HLF procedures .