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BRF对局灶性脑梗死大鼠脑组织IGF-1表达的影响
引用本文:刘薇,张祥建,狄楠,胡明,崔海瑛,闫国华,徐启旺,刘俊康,刘瑞春,马惠莉. BRF对局灶性脑梗死大鼠脑组织IGF-1表达的影响[J]. 脑与神经疾病杂志, 2008, 16(4): 328-331
作者姓名:刘薇  张祥建  狄楠  胡明  崔海瑛  闫国华  徐启旺  刘俊康  刘瑞春  马惠莉
作者单位:河北医科大学第二医院神经内科,石家庄,050000;第三军医大学医学检验系生物波实验室;河北医科大学第二医院核医学科,石家庄,050000
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。

关 键 词:脑梗死  大鼠  IGF-1  BRF

The effect of BRF on IGF-1 expression after middle cerebral artery occlusion in rats
Affiliation:LIU Wei,ZHANG Xiang-jian,DI Nan,et al.(Department of Neurology,The Second Hospital of Hebei-Medical University Shijiazhuang,050000)
Abstract: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.
Keywords:cerebral infarction rats IGF-1 BRF
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