摘要
目的探讨Notch信号通过在肢体远程预处理脑缺血中的神经保护作用。方法将大脑中动脉阻闭120分钟(MCAO)制备大鼠局灶性脑缺血模型,将36只雄性SD大鼠随机分为假手术组(Sham)、MCAO组和肢体远端缺血预处理(RIPC)组+MCAO组(n=12),分别观察各组大鼠脑梗死灶的大小和神经功能学评分,并用免疫组织化学染色检测再灌注2 h、24 h、72 h大鼠脑组织纹状体区Notch信号通路胞内活化片段NICD(Notch intracellular domain)表达的变化。结果 RIPC组脑梗死容积小于MCAO组,差异有统计学意义(P<0.05),其神经功能学评分也明显优于MCAO组(P<0.05)。各时相点RIPC组Notch表达明显少于MCAO组(P<0.05)。结论肢体远程预处理所诱导的脑缺血耐受的机制可能与Notch信号表达的降低有关。
Objective To investigate the role of Notch signaling in the neuroprotection after remote ischemic preconditioning （RIPC） in rat model of local cerebral ischemia. Methods Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion （MCAO） for 120 min to establish a local cerebral ischemic model. A total of 36 male rats were randomly assigned to three groups （n = 12）： sham group, MCAO group, and RIPC ＋ MCAO group. Infarction volume of the brain tissue and neurologic scores were evaluated. At 2 h, 24 h and 72 h after reperfusion, the rats were sacrificed and the corpus striatum was dissected for immunohistochemistry to detect the expression changes of Notch intracellular domain （NICD）. Results The infarct volume in RIPC group was smaller than that in MCAO group （P 0.05）, and the neurological dysfunction scores in RIPC group were higher than those in MCAO group （P 0. 05）. At each time point after reperfusion, the expression of Notch signal was obviously less in RIPC group than in MCAO group （P 0.05）. Conclusion RIPC can induce brain ischemia tolerance, which may be related with the decrease of expression of Notch signal.
出处
《中华神经外科疾病研究杂志》
CAS
2011年第3期214-217,共4页
Chinese Journal of Neurosurgical Disease Research
基金
国家自然科学基金资助项目(30930091)
