2002Unpublished venueRequires access

Neuronal apoptosis and protective effect of nerve growth factor in hippocampal CA1 region after cerebral ischemia in rats

Jian Xiong

Open publisher page 0 citations

Abstract

Objective To investigate the mechanism underlying apoptosis and protective effect of nerve growth factor (NGF) in hippocampal CA1 region after cerebral ischemia/reperfusion. Methods Wistar rats were inflicted with four vessel occlusion for global ischemia, and those in NGF group were given intraventricular injection of NGF after ischemia. Immunohistochemistry staining was used to detect P75NTR, Bcl 2 and Bax, and TUNEL method to detect apoptosis. Results The expression of Bax was positive, while the apoptosis and the expressions of P75NTR and Bcl 2 were negative in normal control. After ischemia/reperfusion, the expression of Bcl 2 was still negative, while the expression of P75NTR and Bax increased and reached its summit in day 3. TUNEL positive neurons were seen in day 2 and reached a peak in day 3. In NGF group, the expression of Bcl 2 was increased, while the expression of Bax, P75NTR and TUNEL positive cells were obviously decreased. Conclusion These findings suggest that the increased expression of P75NTR and Bax in hippocampal CA1 region after cerebral ischemia/reperfusion may be one of the main reasons for apoptosis after ischemia. Intraventricular NGF might have protective effect on neuronal apoptosis after cerebral ischemia via regulation the expression of Bcl 2 and Bax by regulated NGF receptor.

About this research paper

What this paper is about

Objective To investigate the mechanism underlying apoptosis and protective effect of nerve growth factor (NGF) in hippocampal CA1 region after cerebral ischemia/reperfusion. Methods Wistar rats were inflicted with four vessel occlusion for global ischemia, and those in NGF group were given intraventricular injection of NGF after ischemia. Immunohistochemistry staining was used to detect P75NTR, Bcl 2 and Bax, and TUNEL method to detect apoptosis. Results The expression of Bax was positive, while the apoptosis and the expressions of P75NTR and Bcl 2 were negative in normal control. After ischemia/reperfusion, the expression of Bcl 2 was still negative, while the expression of P75NTR and Bax increased and reached its summit in day 3. TUNEL positive neurons were seen in day 2 and reached a peak in day 3. In NGF group, the expression of Bcl 2 was increased, while the expression of Bax, P75NTR and TUNEL positive cells were obviously decreased. Conclusion These findings suggest that the increased expression of P75NTR and Bax in hippocampal CA1 region after cerebral ischemia/reperfusion may be one of the main reasons for apoptosis after ischemia. Intraventricular NGF might have protective effect on neuronal apoptosis after cerebral ischemia via regulation the expression of Bcl 2 and Bax by regulated NGF receptor.

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 investigate the mechanism underlying apoptosis and protective effect of nerve growth factor (NGF) in hippocampal CA1 region after cerebral ischemia/reperfusion. Methods Wistar rats were inflicted with four vessel occlusion for global ischemia, and those in NGF group were given intraventricular injection of NGF after ischemia. Immunohistochemistry staining was used to detect P75NTR, Bcl 2 and Bax, and TUNEL method to detect apoptosis. Results The expression of Bax was positive, while the apoptosis and the expressions of P75NTR and Bcl 2 were negative in normal control. After ischemia/reperfusion, the expression of Bcl 2 was still negative, while the expression of P75NTR and Bax increased and reached its summit in day 3. TUNEL positive neurons were seen in day 2 and reached a peak in day 3. In NGF group, the expression of Bcl 2 was increased, while the expression of Bax, P75NTR and TUNEL positive cells were obviously decreased. Conclusion These findings suggest that the increased expression of P75NTR and Bax in hippocampal CA1 region after cerebral ischemia/reperfusion may be one of the main reasons for apoptosis after ischemia. Intraventricular NGF might have protective effect on neuronal apoptosis after cerebral ischemia via regulation the expression of Bcl 2 and Bax by regulated NGF receptor.

Key concepts: TUNEL assay, Nerve growth factor, Ischemia, Hippocampal formation, Apoptosis, Medicine, Immunohistochemistry, Endocrinology

Related papers

Back to paper searchBrowse research topicsOriginal source
Neuronal apoptosis and protective effect of nerve growth factor in hippocampal CA1 region after cerebral ischemia in rats — Research Paper | ScholarLens