氯胺酮对兔全脑缺血-再灌注海马细胞凋亡及TNF-β和IL-10的影响  

Effect of ketamine on apoptosis and TNF-β,IL-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits

作　　者：张全云[1] 丁月东[1] 汪允珍[1] 赵保建[1] 曾永恒[1] 陈前芬[2] 

机构地区：[1]江苏省连云港市第二人民医院麻醉科,222000 [2]安徽蚌埠医学院病理生理学教研室

出　　处：《临床麻醉学杂志》2012年第12期1226-1228,共3页Journal of Clinical Anesthesiology

基　　金：安徽省蚌埠医学院科研项目(BY1055)

摘　　要：目的研究氯胺酮对兔全脑缺血-再灌注损伤中海马细胞凋亡及肿瘤坏死因子β(TNF-β)、白细胞介素-10(IL-10)表达的影响。方法新西兰大白兔45只,随机分为三组,每组15只。A组仅分离股动脉、股静脉和双侧颈总动脉。B组和C组采用股动脉放血,夹毕颈总动脉30min制作全脑缺血-再灌注模型。C组经股静脉推注氯胺酮4.5mg/kg。取海马组织行HE染色、TUNEL、免疫组化染色,计数CA1区存活细胞、凋亡细胞、TNF-β和IL-10阳性细胞个数。结果再灌注后12～72h,C组存活细胞明显多于B组(P<0.05),凋亡细胞明显少于B组(P<0.01)。再灌注后6～72h,B、C组TNF-β明显高于A组(P<0.05)。再灌注后6h和72h,C组TNF-β明显少于B组(P<0.05)。再灌注后6h,C组IL-10阳性细胞数明显多于A、B型,再灌注后72h明显少于A、B组(P<0.05)。结论氯胺酮可通过调节细胞免疫应答,减轻炎症反应,减少细胞坏死和凋亡,具有良好的脑保护作用。Objective To explore the etlect ol Ketamlne on apoptosls ann me expression oi tumor necrosis factor （TNF）-β, interleukin（IL）-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits. Methods Forty-five adult healthy New Zealand white rabbits were equally randomized into three groups （n=15） ： sham operation group （group A）, model group （group B） and model ＋ ketamine group （group C）. The model of global cerebral ischemia-reperfusion was produced by femoral arterial bloodletting combined common carotid occlusion （30 rain）. Ketamine 4. 5 mg/kg was injected through femoral vein after carotid occlusion in group C. The survived neurons in the CA1 region of the hippocampus were observed by HE staining, and apoptosis was detected by TUNEL method. The numbers of TNF-~ and IL-10 positive neurons were detected by immunohistochemical stains. Results Compared with group B, the number of survival cells increased significantly in group C after 12-72 h of reperfusion （P〈0.05） ; the number of apoptosis ceils decreased significantly in group C after 12 72 h of reperfusion （P〈0.01）. The positive expressions of TNF-]3 were higher in group B and C than in group A after 6-72 h of reperfusion（P〈0. 05）, while the positive expressions of TNF-β were lower in group C than in group B after 6 h and 72 h of reperfusion（P〈0.05）. After 6 h of reperfusion, the positive expressions of ILl0 were higher in group C than in group A and B（P〈0.05）, while IL-10 were lower in group C after 72 h of reperfusion（P〈0.05）. Conclusion Ketamine protects brain injury through reducing inflammatory responses and decreasing the necrosis and apoptosis after global cerebral ischem ia-reperfusion in rabbits.

关 键 词：氯胺酮 全脑缺血-再灌注损伤 细胞凋亡 肿瘤坏死因子Β 白细胞介素-10 

分 类 号：R614[医药卫生—麻醉学]