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作 者:韩威[1,2,2] 野向春 孟昭杰 魏胜男[3] 常文光[3]
机构地区:[1]吉林省脑科医院神经内科,吉林四平136000 [2]江苏大学,江苏镇江212013 [3]吉林大学白求恩医学院药理学系,吉林长春132001
出 处:《中风与神经疾病杂志》2012年第6期543-545,共3页Journal of Apoplexy and Nervous Diseases
摘 要:目的探讨尼莫地平对急性脑缺血再灌注损伤的早期保护作用。方法线栓法复制大鼠急性脑缺血模型。30只雄性Wistar大鼠随机分为假手术、模型、尼莫地平3组。模型组采取缺血2h再灌注2h。尼莫地平组大鼠在缺血0时刻起每小时腹腔注射给药一次,剂量为5mg/kg。各组大鼠在手术4h后实验结束后,行腹主动脉采血,同时取完整脑组织。脑组织切片进行TTC染色,并比较各组脑组织梗死面积。检测各组大鼠血清及脑组织匀浆中SOD、MDA、NO含量。结果与模型组相比,尼莫地平组大鼠脑组织梗死面积显著减少。血清生化指标显示,模型组SOD含量显著低于假手术组,给予尼莫地平治疗后,SOD含量增加明显。模型组MDA、NO含量明显高于假手术组,尼莫地平组明显降低血清中MDA、NO。结论尼莫地平对大鼠急性脑缺血再灌注损伤有保护作用,这种保护作用与NO和氧化应激密切相关。Objective To investigate the early protective effect of nimodipine on acute cerebral ischemia reperfusion injury. Methods Focal cerebral ischemia/reperfusion was induced by the middle cerebral artery occlusion (MCAO) meth- od. 30 male Wistar rats were randomly divided into three groups (Sham, Model, Nimodipine teatment group). The model group was induced by 2h ischemia following 2h repeffusion. The nimodipine treatment (5mg/kg) was given at the time of ischemia by intraperitoneal injection once an hour. At the end of the experiment, the abdominal aorta blood was obtained, and full brain tissue was saved. Infarct size by ]~FC staining of brain tissue slices was compared between groups. The activi- ties of SOD, MDA and NO content were detected in serum and brain tissue. Results The infarct size of nimodipine treat- ment group was significantly decreased compared with model group. Serum biochemical indicators suggest that the SOD con- tent of the model group was significantly lower than the sham group, and increased significantly in nimodipine treatment group. MDA and NO content was significantly higher in the Model group than that in the sham group. Nimodipine treatment significantly reduced the serum level of MDA and NO. Conclusion Nimodipine has a protective effect on acute cerebral is- chemia and reperfusion injury, which is closely related to its anti-oxidative stress effect.
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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