高氧液对兔脊髓缺血再灌注损伤的保护作用及对HSP90表达的影响

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目的:寻找新的防止脊髓缺血损伤致瘫痪的手段,研究高氧液对兔脊髓缺血再灌注损伤的保护作用及对热休克蛋白90(heatshockproteinHSP90)表达的影响。方法:雄性新西兰大白兔20只,随机分成对照组n=10)及高氧液组((n=10)。夹闭腹主动脉肾下段20min,建立兔脊髓缺血模型。高氧液组于缺血前20min持续以20mL/kg.h)恒速静脉输入高氧液,直到再灌(注后20min;对照组则采用同种方法静脉输入等容量生理盐水。再灌注后4,8,12,24和48h分别对动物后肢运动功能评分。再灌注48h后,处死动物取脊髓(L5),石蜡包埋切片行组织病理学观察及免疫组织化学染色,并按照McCarthy等的方法对免疫组化染色结果进行分析。结果:高氧液组神经功能评分在各时间点均明显高于对照组(P<0.05);与对照组相比,高氧液组脊髓前角正常神经细胞数明显增多(P<0.01),HSP90的表达高氧液组明显多于对照组(P<0.01)。结论:高氧液对兔脊髓缺血再灌注损伤有显著的保护作用,这种保护机制与脊髓缺血后皮质HSP90表达上调有关。 OBJECTIVE: To find a new means to prevent paralysis caused by spinal cord ischemic injury and to investigate the protective effect of hyperoxia liquid on spinal cord ischemia-reperfusion injury and its effect on the expression of heat shock protein 90 (HSP70). Methods: Twenty male New Zealand white rabbits were randomly divided into control group (n = 10) and hyperoxia group (n = 10) .Close the renal inferior segment of abdominal aorta for 20 minutes to establish a model of spinal cord ischemia in rabbits. 20min / kg.h before ischemia, constant speed intravenous infusion of 20mL / kg.h) until the reperfusion (note 20min; control group is the same method of intravenous infusion of equal volume of saline. 4,8,12 after reperfusion , 24 h and 48 h respectively.After 48 h reperfusion, the animals were sacrificed and the spinal cord (L5) and paraffin embedded sections were taken for histopathological observation and immunohistochemical staining, and immunohistochemistry was performed according to the method of McCarthy et al Results: The neurological scores in hyperoxia group were significantly higher than those in control group at each time point (P <0.05). Compared with control group, the number of normal nerve cells in anterior horn of hyperalgesia group was significantly increased P <0.01), and the expression of HSP90 in hyperoxia group was significantly higher than that in control group (P <0.01) .Conclusion: Hyperoxic liquid has a significant protective effect on spinal cord ischemia-reperfusion injury in rabbits, and this protective mechanism is associated with spinal cord ischemia Post-cortex HSP90 expression is up-regulated.
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