目的 观察信号转导及转录激活因子3（STAT3）磷酸化在树鼩脑缺血后适应(PC) 神经保护中的作用，并探讨其可能机制。 方法 将50只健康成年树鼩随机分为对照组、脑缺血4 h 组、脑缺血24 h 组、后适应4 h 组和后适应24 h 组(每组n=5)，其中10只动物做HE 染色(n=5)及电子显微镜观察(n=5)。本实验通过光化学反应建立树鼩血栓性脑缺血模型；于缺血后4 h夹闭患侧颈总动脉3次（每次5min）实施缺血PC。采用TTC染色观察树鼩脑梗死面积的变化，通过HE和电子显微镜观察脑皮质和海马组织学改变及其超微结构变化，应用Western blotting检测皮层总STAT3（t-STAT3）及磷酸化STAT3(p-STAT3）蛋白表达变化。结果 脑缺血后皮层血管内皮细胞肿胀，皮层及海马神经元损伤，线粒体肿胀、嵴溶解，以缺血24 h损伤最为明显，脑梗死面积达到（24.78±2.06）%。而皮层p-STAT3蛋白表达随缺血时间延长呈增高趋势，缺血4 h p-STAT3蛋白表达明显增高(0.24±0.1, P<0.01），缺血24 h p-STAT3蛋白表达则持续增高(0.32±0.1, P<0.01）。缺血PC处理后皮层血管内皮细胞水肿好转，皮层及海马神经元损伤减轻，脑梗死面积减小为(17.67±1.90)%（P<0.01）。与缺血组相比，缺血PC 4 h p-STAT3蛋白表达进一步升高(0.41±0.09, P<0.01），缺血PC 24 h p-STAT3蛋白表达增高更加显著(0.70±0.11, P<0.01）。 结论 树鼩脑缺血可导致STAT3磷酸化代偿性增强，缺血PC的脑保护作用可能与其促进STAT3过磷酸化有关。

Objective To investigate the regulation of signal transducers and activators of transcription 3(STAT3) phosphorylation in the neuroprotection of ischemic postconditioning(PC) in tree shrews and to explore the neuroprotection mechanisms of ischemic PC. Methods Tree shrews were randomly grouped into control，ischemia 4 hours，ischemia 24 hours，ischemic PC 4 hours and ischemic PC 24 hours (n=5). Ten animals were used for HE staining(n=5) and electron microscopy (n=5)．The model of thrombotic cerebral ischemia was induced by photochemical reaction in tree shrews and the ischemic PC was established at hour 4 after ischemia followed by clipped ipsilateral common caroyid artery on the ischemia side (5 minutes×3). The changes of cerebral infarction area were measured with TTC staining. The histological and ultrastructural changes of cortex and hippocampus were observed by HE staining and electron microscope,respectively. The expression of total STAT3 (t-STAT3) and phosphorylated STAT3(p-STAT3) protein in the cortical tissue were detected by Western blotting. Results The ischemic group showed cortical vascular endothelial cell edema, cortical and hippocampal neurons pycnosis, mitochondrial swelling and partial disrupt, the damage was obvious and the cerebral infarction area was (24.78±2.06)% at hour 24 after cerebral ischemia. With the time prolonging of ischemia, the phosphorylation of STAT3 in the cortical neurons was significantly increased (0.24±0.1, P<0.01）at hour 4 and increased continuously (0.32±0.1, P<0.01）at hour 24 after cerebral ischemia. But the damage of vascular endothelial cell and neurons was alleviated and the cerebral infarction area was decreased (17.67±1.90)% (P<0.01）at hour 24 after ischemic PC. Compared with the ischemia group, the phosphorylation of STAT3 was further increased at hour 4 (0.41±0.09, P<0.01）and was significantly increased at hour 24 (0.70±0.11, P<0.01）after ischemic PC. Conclusion Cerebral ischemia may lead to compensatory increase of STAT3 phosphorylation and the neuroprotection of ischemic PC may be related to the promotion of STAT3 phosphorylation in tree shrews.