2007•Shiyong yixue zazhiRequires access

Study on neuronal apoptosis and Bcl-2 gene expression after forebrain ischemia-reperfusion in rats

Yan Hu

Open publisher page 0 citations

Abstract

Objective To observe the changes of Bcl-2 expression in apoptosis of neurons and to investigate the molecular mechanism of apoptosis following forebrain cerebral ischemia-reperfusion. Methods Twenty-one male SD rats were randomly divided into 7 groups: control group,1,3,6,12,24,48 h after focal cerebral ischemia-reperfusion group. The neuronal apoptosis in the hippocampus after forebrain ischemia-reperfusion was detected by terminal deoxynuleotide transferase-mediated dUTP nick end labeling (TUNEL) technique and the changes in Bcl-2 expression were determined using immunohistochemical method. Results The apoptotic cells in the hippocampus appeared at 6 h after forebrain ischemia-reperfusion,peaked at 24 h,and then decreased. Bcl-2 gene was positively expressed at 1 h and the expression reached its peak level at 12 h,and then declined to a lower level. Conclusion The expression of Bcl-2 protein plays a vital role in the process of neuronal apoptosis.

About this research paper

What this paper is about

Objective To observe the changes of Bcl-2 expression in apoptosis of neurons and to investigate the molecular mechanism of apoptosis following forebrain cerebral ischemia-reperfusion. Methods Twenty-one male SD rats were randomly divided into 7 groups: control group,1,3,6,12,24,48 h after focal cerebral ischemia-reperfusion group. The neuronal apoptosis in the hippocampus after forebrain ischemia-reperfusion was detected by terminal deoxynuleotide transferase-mediated dUTP nick end labeling (TUNEL) technique and the changes in Bcl-2 expression were determined using immunohistochemical method. Results The apoptotic cells in the hippocampus appeared at 6 h after forebrain ischemia-reperfusion,peaked at 24 h,and then decreased. Bcl-2 gene was positively expressed at 1 h and the expression reached its peak level at 12 h,and then declined to a lower level. Conclusion The expression of Bcl-2 protein plays a vital role in the process of neuronal apoptosis.

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 observe the changes of Bcl-2 expression in apoptosis of neurons and to investigate the molecular mechanism of apoptosis following forebrain cerebral ischemia-reperfusion. Methods Twenty-one male SD rats were randomly divided into 7 groups: control group,1,3,6,12,24,48 h after focal cerebral ischemia-reperfusion group. The neuronal apoptosis in the hippocampus after forebrain ischemia-reperfusion was detected by terminal deoxynuleotide transferase-mediated dUTP nick end labeling (TUNEL) technique and the changes in Bcl-2 expression were determined using immunohistochemical method. Results The apoptotic cells in the hippocampus appeared at 6 h after forebrain ischemia-reperfusion,peaked at 24 h,and then decreased. Bcl-2 gene was positively expressed at 1 h and the expression reached its peak level at 12 h,and then declined to a lower level. Conclusion The expression of Bcl-2 protein plays a vital role in the process of neuronal apoptosis.

Key concepts: TUNEL assay, Apoptosis, Forebrain, Ischemia, Hippocampus, Immunohistochemistry, Biology, Gene expression

Related papers

Back to paper searchBrowse research topicsOriginal source
Study on neuronal apoptosis and Bcl-2 gene expression after forebrain ischemia-reperfusion in rats — Research Paper | ScholarLens