内源性IGF-1有利于短暂脑缺血损伤新生大鼠海马神经发生  

Endogenous insulin growth factor-1 contributes to hippocampal neurogenesis in neonatal rats with transient forebrain ischemia

作　　者：曾文钦[1] 刘钦[1] 姚前尹[1] 程亚涛[1] 戴景兴[2] 原林[2] 

机构地区：[1]广东嘉应学院医学院人体解剖学教研室,广东梅州514031 [2]南方医科大学人体解剖学教研室,广东广州510515

出　　处：《广州医学院学报》2014年第1期5-9,共5页Academic Journal of Guangzhou Medical College

基　　金：国家重点基础研究计划(973计划)项目(2007CB512705);国家自然科学基金青年面上项目(30801464)

摘　　要：目的:7日龄新生大鼠短暂脑缺血诱导海马齿状回(dentate gyrus,DG)新生细胞增殖,观察内源性IGF-1对新生细胞增殖的影响。方法:7日龄新生大鼠64只随机分为缺血(BCCA0)组(n=24)、假手术(SS)组(n=24)、缺血阻断剂(BCCAO+JB1)组(n=8)和缺血生理盐水(BCCA0+SS)组(n=8)。用免疫组织化学方法观察BCCAO组和SS组在缺血再灌注后1、4、7 d DG区新生细胞和IGF-1的增殖变化;观察BCCA0+SS组和BCCAO+JB1组在IGF-1受体阻断剂(JB1)阻断7 d后DG区新生细胞和IGF-1的增殖变化。结果:与同时间点SS组比较,缺血再灌注后1、4、7 d的DG区新生细胞和IGF-1阳性细胞数目均显著增加,差异有统计学意义(P<0.05);BCCA0+JB1组IGF-1的表达被阻断,IGF-1阳性细胞数目缺如,而BCCA0+SS组IGF-1表达如常;BCCAO+JB1组DG区新生细胞数目显著减少,与BCCA0+SS组相比,差异有统计学意义(P<0.05)。结论:新生大鼠缺血再灌注损伤上调内源性IGF-1的表达,从而促使DG区新生细胞增殖;使用JB1后,IGF-1的表达被阻断,DG区新生细胞增殖也显著减少,提示内源性IGF-1有利于短暂脑缺血损伤新生大鼠海马区域的神经发生。Objective:To study the impacts of endogenous insulin-like growth factor-1(IGF-1) on hippocampus dentate gyrus(DG) cell proliferation,induced by transient forebrain ischemia,at postnatal day 7in neonatal rats.Methods:Sixty-four neonatal rats at postnatal day 7 were randomly assigned to ischemia group(BCCAO,n = 24),sham group(SS,n = 24),ischemia antagonist treatment group(BCCAO+JB1,n = 8) and ischemia plus saline injection group(BCCAO+SS,n=8),respectively.The cell proliferation and IGF-1 in the DG of groups BCCAO and SS were observed on days 1,4 and 7 after ischemia by using immunohistochemical staining.The cell proliferation and IGF-1 in the DG of groups BCCAO+JB1 and BCCAO+SS were detected at day7.Results:Compared with group SS,reperfusion following ischemia resulted in significantly increased number of BrdU+ cells and IGF-l+cells in the DG of BCCAO group at days 1,4 and 7(all P<0.05).The administration of JB1 led to blockade of IGF-1 expression and lack of IGF-l+cells in group BCCA0+JB1,but not group BCCAO+SS.The number of BrdU+ cells in the DG of BCCAO+JB1 group was markedly decreased compared with group BCCAO+SS(P<0.05).Conclusion:Ischemia/reperfusion injury up-regulates the expression of IGF-1 in neonatal rats leading to cell proliferation.The blockade of IGF-1 and diminished cell proliferation in the DG following the administration of JB1 suggest that endogenous IGF-1 contributes to hippocampal neurogenesis in neonatal rats with transient forebrain ischemia.

关 键 词：短暂脑缺血 神经发生 胰岛素样生长因子1 免疫组织化学 新生大鼠 

分 类 号：R364.4[医药卫生—病理学]