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环孢素A对大鼠脑缺血再灌注后IL-1β表达的影响 被引量:1

Effect of cyclosporin A on IL-1β expression of cerebral ischemia-reperfusion-injury in rats
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摘要 目的 探讨环孢素A对大鼠脑缺血再灌注损伤后的脑保护作用及其对IL 1β表达的影响。 方法 将 72只大鼠分为假手术组、生理盐水对照组和环孢素A治疗组 ,参照Zealonga线栓法制备局灶性脑缺血再灌注模型 ,大鼠脑缺血 2h再灌注 2 2h和 70h后 ,分别对各组各时间点大鼠进行脑TTC染色评价脑梗死体积、采用RT PCR和放免法分别对缺血区皮层IL 1β基因表达和蛋白表达进行测定。结果 各时间点环孢素A治疗组与生理盐水对照组相比 ,环孢素A治疗组脑梗死灶体积比对照组明显减小 (P <0 .0 5 ) ;环孢素A可有效降低大鼠局灶性脑缺血再灌后脑组织中IL 1β基因和蛋白的表达 (P <0 .0 1) ;与上述两组相比 ,假手术组各项观察指标则无明显异常。结论 IL 1β参与脑缺血再灌注损伤 ,环孢素A对大鼠脑缺血再灌注损伤有明显的保护作用 ,环孢素A的脑保护机制可能与抑制缺血区内IL Objective To explore the protective mechanism of cyclosporin A and investigate the effect of cyclosporin A on IL 1β expression of cerebral ischemia reperfusion injury in rats.Methods 72 wistar rats were randomly divided into 3 groups,which were sham operation group?saline control groups and cyclosporin A treatment group.The models of focal cerebral ischemia reperfusion injury in rats were established with suture method.TTC staining was used to calculate the infarct size. The IL 1β gene expression was determined with RT PCR.The IL 1β protein expression was measured with radioimmunoassay method.Results Compared between the cyclosporin A group and the control group in scheduled time,the cerebral infarct size in cyclosporin A group was markedly lower than that in control group( P < 0.05 );Both the expression of IL 1β gene and IL 1β protein in cyclosporin A group were significantly lower than those in control group( P < 0.01 ).Compared to other two groups,the sham operation group had no obvious abnormal change in each observational item.Conclusions IL 1β takes part in cerebral ischemic reperfusion injury in rats and cyclosporin A possesses protective effect on cerebral ischemic reperfusion injury, which may possibly have effcet of ihibiting IL 1β expression in rats.
出处 《卒中与神经疾病》 2004年第5期289-292,共4页 Stroke and Nervous Diseases
关键词 环孢素A IL-1Β 大鼠 表达 脑缺血再灌注损伤 对照组 治疗组 基因 比对 蛋白 Cyclosporine A Cerebral ischemia reperfusion injury interleukin-1β rat
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参考文献6

  • 1Li PA, Kristian T, He QP, et al. Cyclosporin A enhances survival,aneliorates brain damage, and prevents secondary mitochondrial dysfunction after a 30-minute period of transient cerebral ischemia. Exp Neurol, 2000,165(1 ): 153-163.
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同被引文献10

  • 1储国祥,陈修.脑缺血和脑血流实验方法[M]//徐叔云,卞如濂,陈修.药理实验方法学.第3版.北京:人民卫生出版社,2002:1060-1072.
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  • 5SAITO A,MAIER C M,NARASIMHAN P,et al.Oxidative stress and neuronal death/survival signaling in cerebral ischemia[J],2005,31(1/3):105-116.
  • 6BASU A,LAZOVIC J,KRADY J K,et al.Interleukin-1 and the interleukin-1 type 1 receptor are essential for the progressive neurodegeneration that ensues subsequent to a mild hypoxic/ischemic injury[J].J Cereb Blood Flow Metab,2005,25(1):17-29.
  • 7OPRICA M,ERIKSSON C,SCHULTZBERG M.Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin-1 system[J].J Cell Mol Med,2003,7(2):127-140.
  • 8DIRNAG I U,LADECOLA C,MOSKOWITZ M A.Pathobiology of ischemic stroke:an integrated view[J].Trends Neurosci,1999,22(9):391-397.
  • 9OHTAKI H,FUNAHASHI H,DOHI K,et al.Suppression of oxidative neuronal damage after transient middle cerebral artery occlusion in mice lacking interleukin-1[J].Neurosei Ras,2003,45(3):313-324.
  • 10张晓彪,王建伟,胡卫星,戴建础,崔尧元.插线法制作大鼠大脑中动脉闭塞局灶性脑缺血再灌注模型[J].南京医科大学学报(自然科学版),2001,21(1):32-34. 被引量:7

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