Ischemic preconditioning relieves ischemia/reperfusion injury of hippocampus neurons in rat by inhibiting p53 and bax expressions.

Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih Pub Date : 2007-06-01

Hui-Min Liu, Jing-Xin Li, Lian-Bi Chen

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Abstract

Objective: To examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats, and explore the role of p53 and bax in this process.

Methods: We examined the effect of IPC on delayed neuron death, neuron apoptosis, expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining, flow cytometry, RT-PCR, and immunohistochemistry technique.

Results: IPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216 +/- 9 cells/0.72 mm2 vs. 30 +/- 5 cells/0.72 mm2, P < 0.01) , decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06% +/- 0.21% vs. 4.27% +/- 0.08%, P < 0.01 ), and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC.

Conclusion: IPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ischemia/reperfusion, and this process may be related to the reduced expressions of p53 and bax.

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缺血预处理通过抑制p53和bax的表达减轻大鼠海马神经元缺血再灌注损伤。

目的:探讨缺血预处理(IPC)对大鼠致死性缺血再灌注后海马CA1亚区神经元延迟死亡的保护作用，并探讨p53和bax在这一过程中的作用。方法:采用HE染色、流式细胞术、RT-PCR及免疫组织化学技术检测IPC对大鼠海马CA1区延迟性神经元死亡、神经元凋亡及p53、bax基因表达的影响。结果:IPC增加了海马CA1区存活细胞数量(216 +/- 9个细胞/0.72 mm2 vs. 30 +/- 5个细胞/0.72 mm2, P < 0.01)，降低了海马缺血/再灌注引起的神经元凋亡百分比(2.06% +/- 0.21% vs. 4.27% +/- 0.08%， P < 0.01)，与未IPC的海马缺血/再灌注相比，海马p53、bax基因表达减弱。结论:IPC可保护海马CA1区神经元免受缺血再灌注引起的凋亡，这一过程可能与降低p53和bax的表达有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih

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