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目的探讨高血压对全脑缺血再灌注神经功能的影响及SP600125的干预作用。方法将12周龄42只雄性Wistar-Kyoto(WKY)大鼠随机分为对照组和WKY全脑缺血再灌注组(WKY+缺血再灌注组),同周龄46只雄性自发性高血压大鼠(SHR)随机分为高血压全脑缺血再灌注组(SHR+缺血再灌注组)、高血压全脑缺血再灌注加抑制剂组(抑制剂组)。抑制剂组于缺血前30min侧脑室注射c-Jun氨基末端激酶(JNK)抑制剂SP600125。应用四血管阻断法(Pulsinelli-4VO法)制备全脑缺血模型,脑缺血20min分再灌注24、48h两个时间点,电镜和光镜观察海马区神经细胞形态变化,再灌注48h应用神经功能学检测表评价运动和感觉功能。结果与WKY+缺血再灌注组对比,SHR+缺血再灌注组24、48h神经元细胞形态结构损伤随时间延长加重,神经元细胞存活密度降低(15.56±1.81比22.52±0.96,7.33±1.32比14.11±1.61,均P<0.05)。SHR+缺血再灌注组运动及感觉功能明显低于WKY+缺血再灌注组(4.79±0.93比7.79±0.72,4.42±0.72比6.42±0.65,均P<0.05)。与SHR+缺血再灌注组对比,抑制剂组24、48h神经元细胞形态结构明显改善,细胞存活密度增加(24.11±1.62比15.56±1.81,17.89±1.54比7.33±1.32),抑制剂组运动及感觉功能均明显提高(6.54±0.83比4.79±0.93,5.54±0.66比4.42±0.72,均P<0.05)。结论高血压加重脑缺血再灌注后神经功能的损伤,SP600125对高血压大鼠全脑缺血再灌注损伤有保护作用。
Objective To investigate the effect of hypertension on the neurological function after global cerebral ischemia and reperfusion and the intervention effect of SP600125. Methods Forty-two male Wistar-Kyoto (WKY) rats at 12 weeks of age were randomly divided into control group and WKY group (WKY + ischemia-reperfusion group). 46 male spontaneous hypertensive rats Rats (SHR) were randomly divided into two groups: SHR + ischemia reperfusion group (SHR + ischemia reperfusion group), Hypertensive cerebral ischemia / reperfusion group (inhibitor group). In the inhibitor group, the c-Jun N-terminal kinase (JNK) inhibitor SP600125 was injected into the lateral ventricle 30 min before ischemia. The model of global cerebral ischemia was established by four-vessel occlusion method (Pulsinelli-4VO method). The rats were reperfused for 24 h and 48 h after cerebral ischemia for 20 min. The morphology of neurons in hippocampus was observed by electron microscope and light microscope. Functional test sheets assess motor and sensory functions. Results Compared with WKY + ischemia / reperfusion group, the morphological changes of neurons in SHR + ischemia / reperfusion group were aggravated with time and the survival density of neuronal cells was decreased (15.56 ± 1.81 vs 22.52 ± 0.96, 7.33 ± 1.32 vs 14.11 ± 1.61, all P <0.05). The motor and sensory function of SHR + ischemia-reperfusion group was significantly lower than that of WKY + ischemia-reperfusion group (4.79 ± 0.93 vs. 7.79 ± 0.72, 4.42 ± 0.72 vs. 6.42 ± 0.65, all P <0.05). Compared with SHR + ischemia / reperfusion group, the morphological changes of neurons in 24 h and 48 h of inhibitor group were significantly improved, cell viability increased (24.11 ± 1.62 vs 15.56 ± 1.81, 17.89 ± 1.54 vs 7.33 ± 1.32) Sensory function were significantly improved (6.54 ± 0.83 vs 4.79 ± 0.93, 5.54 ± 0.66 vs 4.42 ± 0.72, all P <0.05). Conclusion Hypertension aggravates neurological damage after cerebral ischemia and reperfusion, and SP600125 has protective effects on global cerebral ischemia-reperfusion injury in hypertensive rats.