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大鼠大脑中动脉短暂闭塞后p53免疫反应性蛋白及p53 mRNA表达

p53-immunoreactive protein and p53 mRNA expression after transient middle cerebral artery occlusion in rats.

作者信息

Li Y, Chopp M, Zhang Z G, Zaloga C, Niewenhuis L, Gautam S

机构信息

Department of Neurology, Henry Ford Hospital Health Science Center, Detroit, Mich.

出版信息

Stroke. 1994 Apr;25(4):849-55; discussion 855-6. doi: 10.1161/01.str.25.4.849.

Abstract

BACKGROUND AND PURPOSE

We investigated the temporal distribution of the p53-immunoreactive protein in conjunction with cellular damage and the expression of the p53 mRNA after focal cerebral ischemia in rats.

METHODS

Male Wistar rats (n = 66; controls, n = 7) were subjected to 2 hours of middle cerebral artery occlusion and were killed at various times of reperfusion (0.5 to 168 hours) for p53 immunohistochemistry and Northern blot analysis.

RESULTS

A cellular expression of mutant p53-immunoreactive protein was found localized to anatomic sites exhibiting severe neuronal damage. A maximal induction of mutant p53-immunoreactive protein was found at 12 hours after reperfusion and subsequently declined. No wild-type p53 protein expression was detected after ischemia. A time-dependent expression of p53 mRNA was observed in both hemispheres. The peak level of p53 mRNA occurred at 24 hours after reperfusion.

CONCLUSIONS

Our data indicate that the expressions of p53-immunoreactive protein and p53 mRNA are upregulated after transient focal cerebral ischemic insult in rats. The concomitant appearance of p53 and cell damage in ischemic brain suggests that p53 expression may impact cell biological response to an ischemic insult.

摘要

背景与目的

我们研究了大鼠局灶性脑缺血后p53免疫反应性蛋白的时间分布及其与细胞损伤的关系,以及p53 mRNA的表达情况。

方法

雄性Wistar大鼠(n = 66;对照组,n = 7)接受2小时的大脑中动脉闭塞,在再灌注的不同时间点(0.5至168小时)处死,进行p53免疫组织化学和Northern印迹分析。

结果

发现突变型p53免疫反应性蛋白的细胞表达定位于表现出严重神经元损伤的解剖部位。再灌注后12小时发现突变型p53免疫反应性蛋白的诱导达到最大值,随后下降。缺血后未检测到野生型p53蛋白表达。在两个半球均观察到p53 mRNA的时间依赖性表达。p53 mRNA的峰值水平出现在再灌注后24小时。

结论

我们的数据表明,大鼠短暂局灶性脑缺血损伤后p53免疫反应性蛋白和p53 mRNA的表达上调。缺血脑中p53与细胞损伤同时出现,提示p53表达可能影响细胞对缺血损伤的生物学反应。

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