2006Journal of Brain and Nervous DiseasesRequires access

The relationship between the expression of Bcl-2, Bax protein and apoptosis after cerebral ischemia reperfusion injury

Guilan Li

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Abstract

Objective: The aim of this research is to study the relationship between the expression of Bcl-2, Bax protein and neuronal apoptosis after ischemia reperfusion. Methods: Fifty-six male wistar rats were used in this study. Four-vessel occlusion was used to establish the global cerebral ischemia reperfusion model in the study groups. The brain of rat was removed in1, 6、12、 24、 48、 72 hours respectively after reperfusion. The time-course expression of Bcl-2, Bax protein was detected in hippocampus by using immunohistochemical method in different time spots after reperfusion. Meanwhile, change of neuron apoptosis in hippocampus were detected by the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method in the different time of reperfusion. Results: The number of apoptotic cells increased with the development of reperfusion within 1~48 hours and reached peak at 48h. The expression of Bcl-2 protein appeared at lh after reperfusion, peaked at 12h, and decreased in 24~72h. Immunoreactivity of Bax protein increased with time after reperfusion with peak expression at 48h. The ratio of Bcl-2/Bax gradually increased at the beginning of reperfusion and approached peak at 12h and decreased in the following time. Conclusion: The neuronal cell apoptosis may play an important role in cerebral ischemia reperfusion injury, while the change of Bcl-2/Bax ratio would play a important role in regulating the neuronal survival or death during reperfusion.

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Objective: The aim of this research is to study the relationship between the expression of Bcl-2, Bax protein and neuronal apoptosis after ischemia reperfusion. Methods: Fifty-six male wistar rats were used in this study. Four-vessel occlusion was used to establish the global cerebral ischemia reperfusion model in the study groups. The brain of rat was removed in1, 6、12、 24、 48、 72 hours respectively after reperfusion. The time-course expression of Bcl-2, Bax protein was detected in hippocampus by using immunohistochemical method in different time spots after reperfusion. Meanwhile, change of neuron apoptosis in hippocampus were detected by the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method in the different time of reperfusion. Results: The number of apoptotic cells increased with the development of reperfusion within 1~48 hours and reached peak at 48h. The expression of Bcl-2 protein appeared at lh after reperfusion, peaked at 12h, and decreased in 24~72h. Immunoreactivity of Bax protein increased with time after reperfusion with peak expression at 48h. The ratio of Bcl-2/Bax gradually increased at the beginning of reperfusion and approached peak at 12h and decreased in the following time. Conclusion: The neuronal cell apoptosis may play an important role in cerebral ischemia reperfusion injury, while the change of Bcl-2/Bax ratio would play a important role in regulating the neuronal survival or death during reperfusion.

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Available abstract

Objective: The aim of this research is to study the relationship between the expression of Bcl-2, Bax protein and neuronal apoptosis after ischemia reperfusion. Methods: Fifty-six male wistar rats were used in this study. Four-vessel occlusion was used to establish the global cerebral ischemia reperfusion model in the study groups. The brain of rat was removed in1, 6、12、 24、 48、 72 hours respectively after reperfusion. The time-course expression of Bcl-2, Bax protein was detected in hippocampus by using immunohistochemical method in different time spots after reperfusion. Meanwhile, change of neuron apoptosis in hippocampus were detected by the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method in the different time of reperfusion. Results: The number of apoptotic cells increased with the development of reperfusion within 1~48 hours and reached peak at 48h. The expression of Bcl-2 protein appeared at lh after reperfusion, peaked at 12h, and decreased in 24~72h. Immunoreactivity of Bax protein increased with time after reperfusion with peak expression at 48h. The ratio of Bcl-2/Bax gradually increased at the beginning of reperfusion and approached peak at 12h and decreased in the following time. Conclusion: The neuronal cell apoptosis may play an important role in cerebral ischemia reperfusion injury, while the change of Bcl-2/Bax ratio would play a important role in regulating the neuronal survival or death during reperfusion.

Key concepts: TUNEL assay, Apoptosis, Ischemia, Reperfusion injury, Immunohistochemistry, BAX Protein, Hippocampus, Neuron

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