尼莫地平激活PI3K/Akt通路对I/R老龄大鼠脑微血管生成机制研究  被引量:3

Research in effects of nimodipine which adjust the PI3K/Akt axis on microvascular generation after cerebral ischemia reperfusion in aged rats

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作  者:余翔[1] 梁辉[1] 曾凯敏[1] 刘昕[1] 彭熠[1] 李春花 傅可[1] YU Xiang;LIANG Hui;ZENG Kai-min;LIU Xin;PENG Yi;LI Chun-hua;FU Ke(Department of Neurology,Hunan People s Hospital,Changsha 410005,Hunan,China)

机构地区:[1]湖南省人民医院神经内科,湖南长沙410005

出  处:《川北医学院学报》2019年第1期19-23,27,共6页Journal of North Sichuan Medical College

基  金:湖南省科技厅科研项目(2008SK3057)

摘  要:目的:研究尼莫地平对脑缺血再灌注老龄大鼠脑微血管生成的影响及可能的作用机制。方法:将SD大鼠随机分为4组:假手术组(n=6)、模型组(n=24)、尼莫地平干预组(n=24)、PI3K/Akt信号通路抑制剂组(n=24),再将后两组大鼠根据缺血(I)/再灌注(R)时间不同分别分为I3 h、I/R1 d、I/R3 d及I/R6 d组,每组6只。采用免疫组织化学方法检测各组大鼠大脑皮质区半暗带微血管α-SMA、PI3K及Akt的表达水平。结果:与假手术组比较,模型组、尼莫地平组和抑制剂组I3 h、I/R1 d、I/R3 d、I/R6 d各时间点的α-SMA、PI3K及Akt阳性表达水平均显著升高(P<0.05);与模型组相同时间点比较,尼莫地平组的α-SMA、PI3K及Akt阳性表达水平均显著升高(P<0.05);与尼莫地平组相同时间点比较,抑制剂组的α-SMA、PI3K及Akt阳性表达水平均显著降低(P<0.05)。结论:随着脑I/R损伤时间的延长,老龄大鼠脑组织内微血管生成标记物α-SMA蛋白的表达逐渐升高;尼莫地平脑组织保护作用可能与提高脑缺血半暗带区α-SMA、PI3K、Akt的表达水平,激活PI3K/Akt信号转导通路,促进血管生成有关。Objective:To investigate the effects of nimodipine on brain microangiogenesis in aging rats with cerebral ischemia-reperfusion and its possible mechanism.Methods:SD rats were randomly divided into 4 groups:sham operation group(n=6),model group(n=24),nimodipine intervention group(n=24),PI3 K/Akt signaling pathway inhibitor group(n= 24),and the latter two groups were divided into I3 h,I/R1 d,I/R3 d and I/R6 d groups according to the time of ischemia(I)/reperfusion(R),respectively,with 6 rats in each group.The expression levels of α-SMA,PI3 K and Akt in the penumbra of the cerebral cortex of each group were detected by immunohistochemistry.Results:Compared with the sham operation group,the expression of α-SMA,PI3 K and Akt were significantly higher in the model group,nimodipine group and inhibitor group at I3 h,I/R1 d,I/R3 d and I/R6 d(P<0.05).The expression of α-SMA,PI3 K and Akt in the nimodipine group were significantly increased than model group at the same time point(P<0.05).The expression of α-SMA,PI3 K and Akt in the inhibitor group were significantly increased than nimodipine group at the same time point(P<0.05).Conclusion:With the prolongation of brain I/R injury time,the expression of microangiogenesis marker α-SMA protein in aged rats increases gradually.The protective effect of nimodipine on brain tissue may be related with the higher expression of SMA,PI3 K and Akt,which activate the PI3 K/Akt1 signal transduction pathway,and then promote angiogenesis.

关 键 词:缺血再灌注 脑微血管生成 PI3K/AKT信号通路 尼莫地平 

分 类 号:R-332[医药卫生]

 

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