期刊文献+

BRF对局灶性脑梗死大鼠脑组织IGF-1表达的影响 被引量:1

The effect of BRF on IGF-1 expression after middle cerebral artery occlusion in rats
下载PDF
导出
摘要 目的:探讨生物波调控因子BRF(Bio-wave regulationfactor)对实验性脑梗死大鼠脑组织中IGF-1表达水平的影响。方法:健康雄性SD大鼠90只,制成大脑中动脉梗死(MCAO)模型,随机分为3组,即BRF组、生理盐水和假手术组,各组又分为6,24,48,72h,7d5个亚组。BRF组为腹腔注射给药,生理盐水组给同体积的生理盐水,于相应时间点进行行为学评分、脑含水量及脑组织中IGF-1的表达。结果:①组织含水量:与假手术组相比,其他各组在各时间段均增加。其中术后48hBRF组低于同期的生理盐水组,P<0.05。②IGF-1阳性细胞表达:与假手术组相比,其他各组在各时间段均增加,梗死后6h开始增多,72h达高峰。术后72hBRF组高于同期的生理盐水组,P<0.05。结论:BRF可促进IGF-1表达,升高脑组织IGF-1含量,减轻局灶性脑梗死引起的缺血性损伤。 Objective:To investigate the effect of Bio-wave regulation factor(BRF)on insulin-like growth factor-1(IGF-1)expression in rats after middle cerebral artery occlusion(MCAO).Methods:A total of 90 adult male Sprague-Dawley rats were subjected to MCAO,and they were randomly divided into sham operation group、normal saline group and BRF treatment group.Each group consisted of 5 subgroups(6 h、24 h、48 h、72 h and 7d),according to different time points post-ischemia,The neurological deficit score(NDS)was assessed with 4 different methods,IGF-1 expression detected by immunohistochemistry method.Results:The amounts of IGF-1 positive cells increased at 6 h,with the peak at 72 h,and continued to 7 d,as well as the inflammatory cell infiltration in the infarction regions,There were several IGF-1 positive cells and no inflammatory cell infiltrating observed in the sham group.The NDS decreased and the histopathologic damages were alleviated with the BRF administration.The expression of IGF-1 was inhibited,significantly at 72 h(P〈0.05).Conclusion:The results suggest that BRF can produce neuroprotective effects on the infarction damage by attenuating the brain edema and inhibiting the expression of IGF-1.
出处 《脑与神经疾病杂志》 2008年第4期328-331,共4页 Journal of Brain and Nervous Diseases
关键词 脑梗死 大鼠 IGF-1 BRF cerebral infarction rats IGF-1 BRF
  • 相关文献

参考文献13

二级参考文献49

  • 1各类脑血管疾病诊断要点[J].中华神经科杂志,1996,29(6):379-380. 被引量:33022
  • 2[2]Altumbabic M, Peeling J, Bigio MRD, et al. Intracerebral hemorrhage in the rat: effects of hematoma aspiration. Stroke,1998,29:1917~1923
  • 3[3]Sansing LH, Kaznatcheeva EA, Perking CJ, et al. Edema after intracerebral hemorrhage: correlation with coagulation parameters and treatment. J Neurosug, 2003,98(5):985~992
  • 4[6]Hua Y, Schallert T, Keep RF, et al. Behavioral tests after intracerebral hemorrhage in the rat. Stroke,2002,33(10):2478~2484
  • 5[7]Yang GY, Betz AL, Chenevert TL,et al. Experimental intracerebral hemorrhage: relationship between brain edema, blood flow, and blood-brain barrier permeability in rats. J Neurosurg 1994,81(1):93~102
  • 6[8]Lee KR, Betz AL, Kim S, et al. The role of the coagulation cascade in brain edema formation after intracerebral hemorrhage. Acta Neurochir, 1996,138(2):396~401
  • 7[9]Bullock R, Mendelow AD, Teasdale GM, et al. Intracranial hemorrhage induced at arterial pressure in the rat. Part 1 Description of technique, ICP changes and neuropathological findings. Neurol Res, 1984,6:184~188
  • 8[10]Xi GH, Hua Y, Bhasin R et al. Stroke, 2001;32(11):2932~2940
  • 9[11]Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniotomy in rats. Stroke, 1989;20(1):84~91
  • 10[12]Sondra T. Bland, BA; Schallert T, et al. Early exclusive use of the affected forelimb after moderate transient focal ischemia in rats: function and anatomic outcome.Stroke,2000,31:1144~1164

共引文献122

同被引文献19

  • 1王楸,陈超,刘登礼,杨毅,陈莲.胰岛素样生长因子-1(IGF-1)对缺氧缺血脑损伤新生鼠内源性IGF-1和IGF-1受体基因表达的影响[J].中国当代儿科杂志,2004,6(6):470-473. 被引量:6
  • 2李玉红,田兆方.不同途径应用胰岛素样生长因子1对新生大鼠缺氧缺血性脑损伤的影响[J].临床神经病学杂志,2005,18(4):285-287. 被引量:3
  • 3刘红锋,孙若鹏,范秀芳,郝素媛,田丽萍.新生儿窒息及缺氧缺血性脑病胰岛素样生长因子1水平变化及临床意义[J].中国新生儿科杂志,2007,22(2):95-96. 被引量:3
  • 4Rice JE, Vannucci RC, Brierley JB. The influence of immaturity on hypoxic-ischemic brain damage in the rat [ J ]. Ann Neuro, 1981, 19(2): 131-141.
  • 5Greenwood SM, Mizielinska SM, Frenguelli BG, Harvey J, Con- nolly CN. Mitochondrial dysfunction and dendritic beading during neuronal toxicity [ J ]. J Biol Chem, 2007, 282 ( 36 ) : 26235- 26244.
  • 6Eldering E, Mackus W J, Derks IA, Evers LM, Beuling E, Teel- ing P, et al. Apoptosis via the B cell antigen receptor requires Bax translocation and involves mitochondrial depolarization, cytochrome C release, and caspase-9 activation [ J]. Eur J Immunol, 2004, 34(7) : 1950-1960.
  • 7Hao Z, Duncan GS, Chang CC, Elia A, Fang M, Wakeham A, et al. Specific ablation of the apoptotic functions of cytochrome C reveals a differential requirement for cytochrome C and Apaf-1 in apoptosis[J]. Cell, 2005, 121(4): 579-591.
  • 8Chandra D, Liu J, Tang DG. Early mitochondrial activation and cytochrome C up-regulation during apoptosis [ J ]. Biol Chem, 2002, 277 (52) : 50842-50854.
  • 9Xia T, Jiang C, Li L, Wu C, Chen Q, Liu SS. A study on perme- ability transition pore opening and cytochrome C release from mito- chondria, induced by caspase-3 in vitro[ J]. FEBS Lett, 2002, 510 (1-2) :62-66.
  • 10Lin S, Fan LW, Pang Y, Rhodes PG, Mitchell HJ, Cai Z. IGF- 1 protects oligodengrocyte projenitor cells and improves neurologi- cal functions following cerebral hypoxia-ischemia in the neontatal rat[J]. Brain Res, 2005, 1063(1) :15-26.

引证文献1

二级引证文献3

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