2006Journal of Brain and Nervous DiseasesRequires access

The expression of Bcl-2/Bax and neuron death after focal cerebral ischemia in rat

Wang Jizuo

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Abstract

Objective:The aim of this study was to investigate the change of Bcl-2 / Bax expression and the neuron death in transient focal cerebral ischemia in rat . Methods: Experimental models of focal ischemia were produced by intra-luminal occlusion of the middle cerebral artery (MCAO) in rats, using immunohistochemical technique in analyzing the expression of Bcl-2 and Bax. The TUNEL staining method was used to characterise the apoptotic cell death. Results: Our results show that the immunoreactivities of both the antiapoptotic agent Bcl-2 and the proapoptotic agent Bax were upreg-ulated, During reperfusion after 2h of ischemia, the expression of Bcl-2 was induced in the ischemic cortex with peak expression at 6h, and then decreased. The expression of Bax was observed markedly in the ischemic cortex at early stage of reperfusion. Immunoreactivity of Bax increased with time after reperfusion with peak expression at 24~48h. The ratio of Bcl-2/ Bax increased at the beginning of reperfusion with peak at 6h, decreasing in the following time. The TUNEL-posi-tive cells were more apparent in the inner border regions immediately adjacent to the ischemic core and progressively increased at 48h. Conclusion: This demonstrates that a specific alteration of the Bax/Bcl-2 ratio would play a vital role in regulating the neuronal survival or death during transient focal cerebral ischemia.

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Objective:The aim of this study was to investigate the change of Bcl-2 / Bax expression and the neuron death in transient focal cerebral ischemia in rat . Methods: Experimental models of focal ischemia were produced by intra-luminal occlusion of the middle cerebral artery (MCAO) in rats, using immunohistochemical technique in analyzing the expression of Bcl-2 and Bax. The TUNEL staining method was used to characterise the apoptotic cell death. Results: Our results show that the immunoreactivities of both the antiapoptotic agent Bcl-2 and the proapoptotic agent Bax were upreg-ulated, During reperfusion after 2h of ischemia, the expression of Bcl-2 was induced in the ischemic cortex with peak expression at 6h, and then decreased. The expression of Bax was observed markedly in the ischemic cortex at early stage of reperfusion. Immunoreactivity of Bax increased with time after reperfusion with peak expression at 24~48h. The ratio of Bcl-2/ Bax increased at the beginning of reperfusion with peak at 6h, decreasing in the following time. The TUNEL-posi-tive cells were more apparent in the inner border regions immediately adjacent to the ischemic core and progressively increased at 48h. Conclusion: This demonstrates that a specific alteration of the Bax/Bcl-2 ratio would play a vital role in regulating the neuronal survival or death during transient focal cerebral ischemia.

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Available abstract

Objective:The aim of this study was to investigate the change of Bcl-2 / Bax expression and the neuron death in transient focal cerebral ischemia in rat . Methods: Experimental models of focal ischemia were produced by intra-luminal occlusion of the middle cerebral artery (MCAO) in rats, using immunohistochemical technique in analyzing the expression of Bcl-2 and Bax. The TUNEL staining method was used to characterise the apoptotic cell death. Results: Our results show that the immunoreactivities of both the antiapoptotic agent Bcl-2 and the proapoptotic agent Bax were upreg-ulated, During reperfusion after 2h of ischemia, the expression of Bcl-2 was induced in the ischemic cortex with peak expression at 6h, and then decreased. The expression of Bax was observed markedly in the ischemic cortex at early stage of reperfusion. Immunoreactivity of Bax increased with time after reperfusion with peak expression at 24~48h. The ratio of Bcl-2/ Bax increased at the beginning of reperfusion with peak at 6h, decreasing in the following time. The TUNEL-posi-tive cells were more apparent in the inner border regions immediately adjacent to the ischemic core and progressively increased at 48h. Conclusion: This demonstrates that a specific alteration of the Bax/Bcl-2 ratio would play a vital role in regulating the neuronal survival or death during transient focal cerebral ischemia.

Key concepts: TUNEL assay, Ischemia, Apoptosis, Immunohistochemistry, Programmed cell death, Neuron, Cortex (anatomy), Middle cerebral artery

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