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大鼠局灶性脑缺血模型海马中bcl-2 mRNA和Bax表达的改变。

Altered expression of bcl-2 mRNA and Bax in hippocampus with focal cerebral ischemia model in rats.

作者信息

Zhang S, Wang W

机构信息

Molecular Medical Center/Department of Neurology, Tongji Hospital, Wuhan 430030, China.

出版信息

Chin Med J (Engl). 1999 Jul;112(7):608-11.

Abstract

OBJECTIVE

Ischemia and reperfusion insults may induce anti-injury response in the sick brain cells, in which regulative genes involved in programmed cell death (PCD) may be activated at the same time. It is attempted to obtain more solid evidence to support the above hypothesis even though the mechanism and pathway of PCD in brain cells after cerebral ischemia has not been identified yet.

METHODS

Focal ischemic model in rats and dot plot hybridization were used to make an observation on the level of bcl-2 mRNA and Bax mRNA expression in the hippocampus cells after a focal ischemic injury, compared to the controls in a pseudo-operation.

RESULTS

Bcl-2 mRNA was remarkably overexpressed in hippocampus area on the ischemic side after 2 hours' ischemia and then 24 hours' reperfusion, but the expression of Bax mRNA was increased without statistically significance. The findings suggested that there was an obvious increase of the expression of the bcl-2 mRNA in the vulnerable area of the brain after a focal ischemia.

CONCLUSION

Bcl-2 may promote the survival of neuron but Bax may induce apoptosis of the cells in hippocampus area of this model. It is also suggested the biologic therapeutic studies, e.g., up-regulation of the expression of the bcl-2 mRNA or down-regulation of expression of the Bax mRNA should be further performed, which may induce the tolerance of the brain cells to the ischemic insult.

摘要

目的

缺血再灌注损伤可能诱导病损脑细胞产生抗损伤反应,在此过程中,参与程序性细胞死亡(PCD)的调控基因可能同时被激活。尽管脑缺血后脑细胞中PCD的机制和途径尚未明确,但仍试图获取更确凿的证据来支持上述假说。

方法

采用大鼠局灶性缺血模型和斑点杂交技术,观察局灶性缺血损伤后海马细胞中bcl-2 mRNA和Bax mRNA的表达水平,并与假手术对照组进行比较。

结果

缺血2小时再灌注24小时后,缺血侧海马区bcl-2 mRNA明显过表达,但Bax mRNA的表达虽有增加但无统计学意义。这些结果提示局灶性缺血后大脑易损区bcl-2 mRNA表达明显增加。

结论

在该模型的海马区,Bcl-2可能促进神经元存活,而Bax可能诱导细胞凋亡。还建议应进一步开展生物学治疗研究,如上调bcl-2 mRNA的表达或下调Bax mRNA的表达,这可能诱导脑细胞对缺血损伤产生耐受性。

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