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目的:观察兔脊髓缺血再灌注后小胶质细胞活化及炎性细胞因子白细胞介素(IL)-6、IL-10、核转录因子(NF)-κB的变化规律,为后处理干预时机提供理论依据。方法:采用胸主动脉球囊阻断法建立兔脊髓缺血再灌注损伤模型。36周健康成年雄性新西兰大白兔54只,假手术组(n=6只)只置入球囊不阻断;48只脊髓缺血再灌注家兔按再灌注时间点分为8组:再灌注0h组、再灌注1h组、再灌注2h组、再灌注3h组、再灌注8h组、再灌注24h组、再灌注48h组、再灌注72h组,每组6只。分别于再灌注后0h、1h、2h、3h、8h、24h、48h和72h检测缺血段脊髓组织中正常神经元、凋亡神经元以及离子钙结合接头分子-1(Iba-1)、IL-6、IL-10、NF-κB的表达水平。结果:正常神经元数量随再灌注时间延长而减少;脊髓缺血再灌注损伤后8h原位末端转移酶标记(TUNEL)阳性神经元开始增多,再灌注24h组的TUNEL阳性神经元达高峰。再灌注2h组的Iba-1表达开始增多,再灌注8h组Iba-1表达达高峰;NF-κB于再灌注3h组开始增高,再灌注8h组NF-κB表达高峰;IL-6和IL-10表达均在再灌注24h组达高峰。脊髓缺血再灌注后NF-κB、IL-6、IL-10的表达水平与Iba-1呈相近的变化趋势。结论:脊髓缺血再灌注后小胶质细胞激活呈动态变化。NF-κB、IL-6、IL-10的表达水平与小胶质细胞激活显著正相关,在小胶质细胞激活前给予后处理可降低神经元损伤。
OBJECTIVE: To observe the changes of microglial activation and inflammatory cytokines interleukin (IL) -6, IL-10 and NF-κB after spinal cord ischemia-reperfusion in rabbits, Provide a theoretical basis. Methods: A rabbit model of spinal cord ischemia-reperfusion injury was established by thoracic aorta balloon occlusion. Fifty-six healthy male New Zealand white rabbits of 36 weeks old were infused into the balloon only in the sham-operation group (n = 6), while 48 rabbits in the spinal cord ischemia-reperfusion group were divided into 8 groups according to the reperfusion time: 0h group, 1h reperfusion group, 2h reperfusion group, 3h reperfusion group, 8h reperfusion group, 24h reperfusion group, 48h reperfusion group and 72h reperfusion group. The normal neurons, apoptotic neurons and Iba-1 in the ischemic segment of spinal cord were detected at 0h, 1h, 2h, 3h, 8h, 24h, 48h and 72h after reperfusion. -6, IL-10, NF-κB expression levels. Results: The number of normal neurons decreased with the prolongation of reperfusion time. TUNEL positive neurons began to increase 8 hours after spinal cord ischemia-reperfusion injury, and TUNEL positive neurons reached the peak at 24 hours after reperfusion. Iba-1 expression began to increase at 2h after reperfusion, and peaked at 8h after reperfusion; NF-κB increased at 3h after reperfusion and peaked at 8h after reperfusion; IL-6 and IL- 10 expression peaked at 24h after reperfusion. The expression of NF-κB, IL-6 and IL-10 in spinal cord ischemia-reperfusion rats were similar to that of Iba-1. Conclusion: The microglial activation changes dynamically after spinal cord ischemia-reperfusion. The expression level of NF-κB, IL-6 and IL-10 was significantly and positively correlated with the activation of microglia. After treatment with microglia, post-treatment could reduce neuronal damage.