期刊文献+

电刺激对脑梗死大鼠运动功能、微管相关蛋白-2和存活素表达的影响 被引量:3

Effects of electrical stimulation on motor function and the expressions of microtubule-associated protein-2 and survivin after cerebral infarction in rats
原文传递
导出
摘要 目的探讨单侧和双侧电刺激对大鼠脑梗死后肢体运动功能和梗死灶周围微管相关蛋白-2(MAP-2)和存活素(survivin)表达的影响。方法128只大鼠随机分为假手术组32只和脑梗死模型组96只。将96只大鼠再随机分为对照组、单侧电刺激组和双侧电刺激组,每组32只。采用线栓法制备大鼠局灶性脑缺血模型,分别接受自然恢复、瘫痪侧电刺激或双侧电刺激治疗3、7、14、21d。电刺激前、后分别用横木行走试验(BWT)检测4组大鼠肢体功能情况,并利用免疫组化染色和苏木素-伊红(HE)染色观察梗死灶周围MAP-2和survivin的表达。结果电刺激治疗后,单侧电刺激组和双侧电刺激组大鼠瘫痪肢体的运动功能较对照组明显改善,双侧电刺激组优于单侧电刺激组。治疗第7天起,单侧电刺激组和双侧电刺激组梗死灶周围脑组织MAP-2表达水平明显高于对照组;治疗第14天起,双侧电刺激组MAP-2的表达水平明显高于单侧电刺激组,治疗第21天双侧电刺激组与假手术组MAP.2表达水平差异无统计学意义(P〉0.05)。单侧电刺激组和双侧电刺激组治疗各时间点梗死灶周围脑组织survivin表达水平明显高于假手术组,治疗第7、14天,survivin表达水平明显高于对照组,达到高峰;而双侧电刺激组明显高于单侧电刺激组;治疗第21天,单侧电刺激组、双侧电刺激组和对照组survivin表达水平有下降,单侧电刺激组与双侧电刺激组间差异无统计学意义(P〉0.05)。结论电刺激不仅能诱导脑梗死大鼠梗死灶周围MAP-2、survivin的表达,而且能促进脑梗死大鼠瘫痪肢体运动功能的恢复,尤其是双侧电刺激的效果优于单侧电刺激,其促进神经功能恢复的机制可能与survivin、MAP-2表达的上调有关。 Objective To investigate the effects of unilateral and bilateral electrical stimulation of the upper and lower limbs on motor function following cerebral infaretion and the expressions of microtubule-associated protein- 2 (MAP-2) and survivin in the infarction border zone of rats. Methods Adult male Sprague-Dawley (SD) rats were randomly divided into sham operation, control, impaired limb and bilateral limbs electrical stimulation groups (each group included 32 rats). Acute cerebral infarction was mimicked using a middle cerebral artery occlusion technique. After cerebral infarction for 24 h, the rats were treated daily with or without electrical stimulation. A beam walking test (BWT) was used to measure limbs motor function and immunohistochemistry and HE staining were used to detect the expressions of MAP-2 and survivin in the border zone of infarcted area after electrical stimulation treatment for 3, 7, ld and 21 d. Results Comparet with the control group treatment with electric stimulation led to BWT scores increasing significantly, and bilateral stimulation was more potent in ameliorating motor function than stimulating the impaired limb only. The expression of MAP-2 was significantly higher in electrical stimulation groups than in control group from the 7th of treatment, and it was higher in bilateral stimulation group than that in unilateral stimulation group from the 14th day of treatment. There was no significant difference in MAP-2 expression between bilateral stimulation group and sham operation group at the 21st day of treatment. In electrical stimulation groups, at every time point the expressions of survivin were obviously higher than that in sham operation group, and it was higher than that in control group and peaked at the 7th and 14th day of treatment and in bilateral stimulation group it was notably higher than that in unilateral stimulation group. At the 21st d of treatment the level of survivin expression dropper; however, there was no significant difference between unilateral and bilateral electrical stimulation groups. Conclusions Treatment with electrical stimulation, particularly in bilateral limbs stimulation, could induce MAP-2 and survivin expressions in the infarction border zone of rats. It also could promote the recovery of motor function in paralyzed limbs after cerebral infarction of rats. The improvement might involve the up-regulation of MAP-2 and survivin expressions.
出处 《中华物理医学与康复杂志》 CAS CSCD 北大核心 2009年第8期514-518,共5页 Chinese Journal of Physical Medicine and Rehabilitation
基金 山东省卫生厅计划课题(2007WH114)
关键词 运动功能 脑梗死 电刺激 微管相关蛋白-2 存活素 Motor function Cerebral infarction Electrical stimulation Microtubule-associated protein-2 Survivin
  • 相关文献

参考文献13

  • 1廖维靖,杨万同,刘淑红,范明,杨运煌,刘买利.线栓阻断大鼠大脑中动脉制作缺血性脑损伤模型的改良[J].中华物理医学与康复杂志,2002,24(6):345-348. 被引量:138
  • 2Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke, 1989,20: 84-91.
  • 3Feeney DM, Gonzalez A, Law WA. Amphetamine, haloperidol and experience interact to affect rate of recovery after motor cortex injury. Science, 1982,217:855-857.
  • 4Maccioni RB, Cambiazo V. Role of microtubule-associated proteins in the control of microcrotubule assembly. Physiol Rev, 1995,75: 835-864.
  • 5Li Y, Jiang N, Powers C, et al. Neuronal damage and plasticity identified by microtubule-associated protein 2, growth-associated protein 43,and cyclin D1 immunoreactivity after focal cerebral ischemia in rats. Stroke, 1998,29 : 1972-1980.
  • 6Conway EM,Zwerts F, Van Eygen V, et al. Survivin-dependent angiogenesis in ischemic brain: molecular mechanisms of hypoxia-induced up-regulation. Am J Pathol,2003 ,163 :935-946.
  • 7蒋祝昌,毕桂南.肾性高血压大鼠局灶性脑缺血再灌注后Survivin表达和细胞凋亡及意义[J].广西医学,2005,27(6):785-787. 被引量:5
  • 8Suzuki A, Ito T, Kawano H, et al. Survivin initiates procaspase3/ p21complex formation as a result of interaction with Cdk4 to resist Fas- mediated cell death. Oncogene, 2000,19 : 1346-1353.
  • 9Tamm I, Wang Y, Sausville E, et al. IAP-family protein surviving inhibits caspase activcity and apoptosis induced by Fas (CD95), Bax, caspases,and anticancer drugs. Cancer Res,1998,58:5315-5320.
  • 10Kobayashi K, Hatano M, Otaki M, et al. Expression of a murine homologue of the inhibitor of apoptosis protein is related to cell proliferation. Proc Natl Acad Sci USA, 1999,96 : 1457-1462.

二级参考文献28

  • 1蒋祝昌,毕桂南,石胜良,王耀明.石蜡线栓的大鼠局灶性脑缺血再灌注模型[J].中国临床神经科学,2004,12(3):303-305. 被引量:9
  • 2Adida C, Crotty PL, Mograth J, et al. Developmentally regulated expression of the novel cancer anti-apoptosis gene Survivin in human and mouse differentiation[J]. Am J Pathol, 1998,152( 1 ) :43~49.
  • 3Tamm T, Wang Y, Sausville E, et al. IAP- Family protein Survivin inhibits caspase activity and apoptosis induced by Fas (CD95), Bax,Caspase and anticancer drugs[ J ]. Cancer Res, 1998,58 (21):5 315 ~5 320.
  • 4Suzuki A, Ito T, Kawano H, et al. Survivin initiates ptrocapase 3/p21complex formation as a result of interaction with CDK4 to resist Fasmediated cell death[J] .Oncogene,2000,19(9): 1 346~1 353.
  • 5Li Y, Chopp M, Jiang N, et al. Temporal profile in situ DNA fragmentation afteir transient middle cerebral artery occlusion in the rat[J].J Cereb Blood Flow Metab, 1995,15(4) :389~397.
  • 6Zhang L,Sarafian T, Kane D, et al. Bcl-2 inhibits death of central nervous cell induced by multiple agents[J ] .Proc Natl Acad Sci USA,1993,90(18) :4 533~4 546.
  • 7Shimizu S, Eguchi Y, Kosaka H, et al. Prevention of hypoxiainduced cell death by Bcl-2 and Bcl-xL[J] .Nature, 1995,374(9):811 ~816.
  • 8Zea Longa E, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke, 1989, 20: 84-9 1.
  • 9Bederson JB, Pitts LH, Tsuji M, et al. Rat middle cerebral art ery occ-lusion: evaluation of the model and development of a neurological e xamination. Stroke, 1986, 17: 472-476.
  • 10Nagasawa H, Kogure K. Correlation between cerebral blood flow and histologic changes in a new rat model of middle cererbal artery occlusion. S troke, 1989, 20: 1037-1043.

共引文献141

同被引文献53

  • 1张光运,曹玉红,许燕,吴中亮,万琪.光化学诱导局灶性脑梗死大鼠小胶质细胞形态变化及环磷酰胺预治疗的作用[J].中国临床康复,2005,9(29):76-77. 被引量:5
  • 2Kiriz M,Lalancette-Hebert M. Inflammation, plasticity and real-time imaging after cerebral ischemia. Acta Neuropathy, 2009,117 : 497- 509.
  • 3longa E Z,Weinstein PR, Carlson S, et al. Reversible middle artery occlusion without craniectomy in rats. Stroke,1989, 20:84-91.
  • 4Wieloch T, Nikolich K. Mechanisms of neural plasticity following brain injury. Curr Opin Neurobiol,2006,16 : 258-264.
  • 5Lakhan SE, Kirchgessner A, Hofer M. Inflammation mechanisms in ischemic stroke: therapeutic approaches. J Transl Med, 2009, 7:97- 114.
  • 6Ekdahl CT, Kokaia Z, Lindval O. Brain inflammation and adult neurogenesis: the dual role of microglia. Neurosciencs, 2009, 158: 1021-1029.
  • 7Zhu J, Qiu Y, Wang Q, et al. Low dose cyclophosphamide rescues myocardial function from ischemia-reperfusion in rats. Eur J Cardiothorac Surg, 2008, 34:661-666.
  • 8Kepermann G, Gast D, Gage FH. Neuroplasticity in old age: sustained fivefold induction of hippocampal neurogenesis by long-term environmental enrichment. Ann Neurol,2002,52 : 135-143.
  • 9Nygren J, Kokaia M, Wieloch T. Decreased expression of brain - derived neurotrophic factor in BNDF(+/-) mice is associated with enhanced recovery of motor performance and increased neuroh|ast member following experimental stroke. J Neurosci Res,2006,84:626- 631.
  • 10Johansson BB, Grabowski M. Functional recovery after brain infraction : plasticity and neural transplation. Brain Pathol, 1994,4 : 85 -95.

引证文献3

二级引证文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部