2009•Chinese Journal of Minimally Invasive NeurosurgeryRequires access

Expression of autophagy-associated protein Beclin 1 in the hippocampus after global brain ischemia-reperfusion injury in rats

Xiaoqiang Wang

Open publisher page 0 citations

Abstract

Objective To study the expression of autophagy-associated protein Beclin 1 and its significance in the hippocampus after global cerebral ischemia-reperfusion injury in rats.Methods The global cerebral ischemia was induced by four-vessel occlusion in Sprague-Dawley(SD) rats.The rats were randomly divided into sham-operated group and ischemia-reperfusion group.Fifteen minutes after the cerebral ischemia,the reperfusion was performed at 0 and 30 min,3,6,12 and 24 h,and 1 and 3 d.The expression of Beclin 1 in the hippocampus after ischemia-reperfusion was detected by immunoblotting analysis at each time point.Results Compared with the sham-operated group,the expression level of Beclin 1 reached a peak at 1 d after cerebral ischemia-reperfusion(P0.05).Conclusion Global cerebral ischemia-reperfusion injury induces up-regulation of Beclin 1 in rat hippocampus,which demonstrates up-regulation of autophagic activity in rat hippocampus after cerebral ischemia and reperfusion.

About this research paper

What this paper is about

Objective To study the expression of autophagy-associated protein Beclin 1 and its significance in the hippocampus after global cerebral ischemia-reperfusion injury in rats.Methods The global cerebral ischemia was induced by four-vessel occlusion in Sprague-Dawley(SD) rats.The rats were randomly divided into sham-operated group and ischemia-reperfusion group.Fifteen minutes after the cerebral ischemia,the reperfusion was performed at 0 and 30 min,3,6,12 and 24 h,and 1 and 3 d.The expression of Beclin 1 in the hippocampus after ischemia-reperfusion was detected by immunoblotting analysis at each time point.Results Compared with the sham-operated group,the expression level of Beclin 1 reached a peak at 1 d after cerebral ischemia-reperfusion(P0.05).Conclusion Global cerebral ischemia-reperfusion injury induces up-regulation of Beclin 1 in rat hippocampus,which demonstrates up-regulation of autophagic activity in rat hippocampus after cerebral ischemia and reperfusion.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Objective To study the expression of autophagy-associated protein Beclin 1 and its significance in the hippocampus after global cerebral ischemia-reperfusion injury in rats.Methods The global cerebral ischemia was induced by four-vessel occlusion in Sprague-Dawley(SD) rats.The rats were randomly divided into sham-operated group and ischemia-reperfusion group.Fifteen minutes after the cerebral ischemia,the reperfusion was performed at 0 and 30 min,3,6,12 and 24 h,and 1 and 3 d.The expression of Beclin 1 in the hippocampus after ischemia-reperfusion was detected by immunoblotting analysis at each time point.Results Compared with the sham-operated group,the expression level of Beclin 1 reached a peak at 1 d after cerebral ischemia-reperfusion(P0.05).Conclusion Global cerebral ischemia-reperfusion injury induces up-regulation of Beclin 1 in rat hippocampus,which demonstrates up-regulation of autophagic activity in rat hippocampus after cerebral ischemia and reperfusion.

Key concepts: Ischemia, Hippocampus, Autophagy, Reperfusion injury, Medicine, Brain ischemia, Anesthesia, Internal medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Expression of autophagy-associated protein Beclin 1 in the hippocampus after global brain ischemia-reperfusion injury in rats — Research Paper | ScholarLens