A的阳性电泳条带(图1)。利用Labworks软件对各阳性条带平均密度进行测量,计算各阳性条带的平均密度值与βactin条带平均密度值之比,结果全脑缺血后1、3、5d胰岛治疗组与缺血组比较无显著差异(表2)。
表2 缺血组及治疗组海马CA1区Bcl2 mRNA的相对含量(略)
Table 2 The relatively content of Bcl2 mRNA of hippocampal CA1 region in ischemic and treated group
*P>0.05 vs. ischemic group
图1 脑缺血后海马CA1区Bcl2 mRNA RTPCR 电泳条带(略)
Fig.1 The electrophoretic strip of Bcl2 mRNA with RTPCR from hippocampal CA1 region post brain ischemic
1, 3, 5: the electrophoretic strip of Bcl2 mRNA of ischemic group in 1,3,5 day, respectively; 2,4,6: the electrophoretic strip of Bcl2 mRNA of insulin treated group in 1,3,5 day, respectively
2.3 全脑缺血后海马CA1区Bcl2蛋白的表达 全脑缺血后1、3、5d,缺血组海马CA1区Bcl2蛋白表达为阴性,而胰岛素治疗组海马CA1区Bcl2蛋白表达则呈阳性(图2)。
2.4 全脑缺血后海马CA1区组织Westernblot结果 全脑缺血后1、3、5d胰岛素治疗组Bcl2蛋白电泳条带密度(图3)均高于缺血组(P<0.01)。表明全脑缺血后经脑室注入胰岛素可提高大鼠海马CA1区Bcl2蛋白的表达(表3)。
表3 海马CA1区Bcl2蛋白电泳条带密度(略)
Table 2 The density of electrophoretic strip of Bcl2 protein from hippocampal CA1 region
*P< 0.01 vs. ischemic group
图2 全脑缺血再灌注后1、3、5d海马CA1区神经元Bcl2蛋白表达(略)
Fig.2 The expression of Bcl2 in hippocampal CA1 region in 1,3,5 day post global brain ischemia (×400)
A-C: the expression of Bcl2 was negative in hippocampal CA1 region in 1,3,5 day post global brain ischemia in ischemic group, respectively;
D-F: the expression of Bcl2 was positive in hippocampal CA1 region in 1,3,5 day post global brain ischemia in insulin treated group, respectively
图3 脑缺血后海马CA1区Bcl2蛋白Westernblot电泳条带(略)
Fig.3 The electrophoretic strip of Bcl2 protein by Westernblot from hippocampal CA1 region post brain ischemia
1: positive control; 2, 4, 6: the electrophoretic strip of Bcl2 protein in 1,3,5 day in ischemic group, respectively; 3,5,7: the electrophoretic strip of Bcl2 protein in 1,3,5 day in insulin treated group, respectively
3 讨论
缺血性脑血管病是威胁人类健康的重大疾病之一,随着对缺血后脑致伤机理研究的深入,目前认为缺血性脑损伤的病理生理机制是一种损伤级
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