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大鼠脑缺血再灌注损伤中环孢素A作用的研究

The Study for the Action of Cyclosporin A on Cerebral Ischemia-Reperfusion-Injury in Rats
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摘要 目的:探讨环孢素A对脑缺血再灌注损伤的保护作用。方法:将108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22h和70h后,分别对各组各时间点大鼠进行行为学评分、细胞凋亡、脑TTC染色和脑超微结构观察,并对结果进行统计处理。结果:各时间点环孢素A治疗组与对照组相比,行为学评分优于对照组(P<0.05);环孢素A处理组脑梗死灶体积和细胞凋亡比例均比对照组明显减轻(P<0.05);环孢素A处理组脑超微结构的异常改变轻于对照组;假手术组各项观察指标则无明显异常改变。结论:免疫因素参与脑的缺血再灌注损伤,环孢素A对实验大鼠脑缺血再灌注损伤具有一定的保护作用。 Objective: To explore the protective action of Cyclosporin A on the cerebral ischemia-reperfusion-in jury in rats. Methods: 108 wistar rats were divided into 3 groups, which were sham operation group,saline control groups and cy-closporin A treatment group. The focal cerebral ischemia-reperfusion-injury model was made by suture occluded method. The behavior obstacles of rats were observed. The cerebral cell apoptosis was detected by flow cytometry. The cerebral slices were stained with TTC methods. The morphological changes in cerebra were observed with the electro-microphones. Results: Compared between the cyclosporin A group and the saline group in scheduled time,the score of behavior obstacles in the cyclosporin A group was better than the saline group(P<0. 05); both the infarct volume and the percentage of cerebral cell apoptosis were markedly decreased than the saline group(P<0. 05) ;the result of electro microphones showed that the morphological changes were less serious in cyclosporin A group compared with the saline group; the sham operation group have no obvious abnormal change in each observational item. Conclusions: The result suggested that the immune factors may play important role in cerebral ischemic reperfusion injury of rats. Cyclosporin A could have protective effect on cerebral ischemic reperfusion injury in rats.
出处 《脑与神经疾病杂志》 2004年第2期99-102,共4页 Journal of Brain and Nervous Diseases
关键词 大鼠 缺血再灌注损伤 脑缺血 环孢素A 免疫因素 cyclosporine A cerebral ischemia reperfusion rat
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  • 1Kobayashi T, Kuroda S, Tada M, et al. Calcium-induced mitochondrial swelling and cytochrome c release in the brain: its biochemical characteristics and implication in ischemic neuronal injury. Brain Res, 2003:960(1-2) :62~70
  • 2Sharkey J, Butcher S P. Immuniphilins mediate the neuroprotective effects of FK506 in focal cerebral ischemia. Nature, 1994,371(3) :336-338
  • 3Uchino H, Minamikawa Tachino R, Kristian T, et al. Neurobiol Dis, 2002,10(3) :219-233
  • 4Li P A, Kristian T, He QP, et al. Exp Neurol, 2000,165(1):153-163
  • 5Matsumoto S, Isshiki A, Watanabe Y, et al. Restricted clinical efficacy of cyclosporin A on rat transient middle cerebral artery occlusion. Life Sci, 2002,20:72(4-5) :591-600
  • 6MacGregor DG, Avshalumov MV, Rice ME. Brain edema induced by in vitro ischemia: causal factors and neuroprotection. J Neurochem, 2003,85(6) :1402-1411
  • 7Zea-Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke,1989,20(2) :84-91
  • 8Rosenberg GA, Scremin O, Estrada E, et al. Arginine vasopressin V1-antagonist and atrial natriuretic peptide reduce hemorrhagic brain edema in rats. Stroke, 1992:23(12):1767-1773
  • 9Swanson RA, Morton MT, Tsao WG, et al. A Semiautomated method for measureing brain infact volume. J Cereb Blood Flow Metab, 1990,10:290-293
  • 10Sinigaglia-Coimbra R, Cavalheiro EA, Coimbra C, et al. J Neurol Sci, 2002,15:203-204:273-276

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