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目的 观察人参皂甙Rb1预处理对大鼠脊髓缺血再灌注损伤后的干预效果,探讨人参皂甙Rb1对抗脊髓缺血再灌注损伤可能的线粒体干预机制.方法 构建大鼠脊髓缺血再灌注损伤模型,随机分为假手术组(n=12)、缺血再灌注损伤组(SCII组,n=12)和人参皂甙Rb1药物组(药物组,n=48),药物组(n=48)又分为10 mg/kg、20 mg/kg、40 mg/kg、80 mg/kg四个亚组,每组12只,术前30 min及术后每天,腹腔注射相应剂量人参皂甙Rb1.各组于损伤后48 h行大鼠后肢神经功能评分;分别检测血清超氧化物歧化酶(SOD)、丙二醛(MDA)含量;取脊髓组织检测SOD、MDA含量以及细胞色素C氧化酶(COX)活性.结果 与SCII组比较,药物组BBB评分升高(P<0.05),血清及脊髓组织SOD含量升高,MDA含量减少,脊髓组织COX活性升高(P<0.05);且呈剂量依赖性,但40 mg/kg与80 mg/kg之间无明显变化.结论 人参皂甙Rb1可以通过抑制线粒体损伤,减轻大鼠脊髓缺血再灌注损伤后的氧化应激,且在10~40 mg/kg范围呈剂量依赖性.“,”Objective To observe the effects of ginsenoside Rb1 pretreatment on spinal cord ischemia-reperfusion injury in rats, and to explore the possible mitochondrial mechanism of ginsenoside Rb1 against ischemia-reperfusion injury. Methods The spinal cord ischemia-reperfusion injury model was established. The rats were randomly divided into sham operation group (n=12), ischemia-reperfusion group (n=12) and drug group (n=12). The drug group received gin-senoside Rb1 peritoneal injection with 10 mg/kg, 20 mg/kg, 40 mg/kg and 80 mg/kg, respectively, 30 minutes be-fore modeling and once a day after modeling. After 48 hours of reperfusion, the BBB score was tested, the levels of superoxide dismutase (SOD) and malonaldehyde (MDA) in the serum and spinal cord tissue, and the cyto-chrome C oxidase (COX) activity in spinal cord tissue were detected. Results Compared with the ischemia-reperfusion group, the BBB score increased (P<0.05), the SOD level increased, and the MDA level decreased both in serum and spinal cord tissue, the activity of COX increased in the spinal cord tissue (P<0.05). All the indexes were dose-dependent, however, no difference was found between 40 mg/kg and 80 mg/kg. Conclusion Ginsenoside Rb1 can inhibit oxidative stress induced by spinal cord ischemia-reperfusion injury in rats by inhibiting mitochondrial damage. The protective effect of ginsenoside Rb1 on the spinal cord ischemia-reperfu- sion injury is dose-dependent during 10 to 40 mg/kg dose.