2005Xinxiang yixueyuan xuebaoRequires access

Observation of hypoxia preconditioning inhibiting the apoptosis in neonatal rats with hypoxic-ischemic brain damage

Tian Mei

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Abstract

Objective To observe the effects of hypoxia preconditioning on the expression of Bcl-2 and Bax in hippocampus of the neonatal rats with hypoxic-ischemic brain damage,and discuss the neruoprotective mechanism of HPC to the HIBD of neonatal rats.Methods Forty 7-day-old Sprague-Dawley rats were randomly divided into control group,sham operated group,hypoxic-ischemic brain damage group(HIBD group) and hypoxia preconditioning group(HPC group).Immunohistochemistry staining was used to examine the expression of Bcl-2 and Bax in hippocampus.Results The amount of the positive cell of Bcl-2 and Bax of HIBD group and HPC group significantly increased compared with that of the control group and sham operated group;The amount of the positive cell of Bcl-2 of HPC group significantly increased and the amount of the positive cell of Bax of HPC group significantly decreased compared with that of HIBD group.Conclusion Hypoxia preconditioning protects cell from apoptosis by promoting the expression of bcl-2,reducing the expression of Bax and adjusting the ratio of Bcl-2/Bax,which would be one of the molecular mechanism of protective role in brain.

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Objective To observe the effects of hypoxia preconditioning on the expression of Bcl-2 and Bax in hippocampus of the neonatal rats with hypoxic-ischemic brain damage,and discuss the neruoprotective mechanism of HPC to the HIBD of neonatal rats.Methods Forty 7-day-old Sprague-Dawley rats were randomly divided into control group,sham operated group,hypoxic-ischemic brain damage group(HIBD group) and hypoxia preconditioning group(HPC group).Immunohistochemistry staining was used to examine the expression of Bcl-2 and Bax in hippocampus.Results The amount of the positive cell of Bcl-2 and Bax of HIBD group and HPC group significantly increased compared with that of the control group and sham operated group;The amount of the positive cell of Bcl-2 of HPC group significantly increased and the amount of the positive cell of Bax of HPC group significantly decreased compared with that of HIBD group.Conclusion Hypoxia preconditioning protects cell from apoptosis by promoting the expression of bcl-2,reducing the expression of Bax and adjusting the ratio of Bcl-2/Bax,which would be one of the molecular mechanism of protective role in brain.

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Available abstract

Objective To observe the effects of hypoxia preconditioning on the expression of Bcl-2 and Bax in hippocampus of the neonatal rats with hypoxic-ischemic brain damage,and discuss the neruoprotective mechanism of HPC to the HIBD of neonatal rats.Methods Forty 7-day-old Sprague-Dawley rats were randomly divided into control group,sham operated group,hypoxic-ischemic brain damage group(HIBD group) and hypoxia preconditioning group(HPC group).Immunohistochemistry staining was used to examine the expression of Bcl-2 and Bax in hippocampus.Results The amount of the positive cell of Bcl-2 and Bax of HIBD group and HPC group significantly increased compared with that of the control group and sham operated group;The amount of the positive cell of Bcl-2 of HPC group significantly increased and the amount of the positive cell of Bax of HPC group significantly decreased compared with that of HIBD group.Conclusion Hypoxia preconditioning protects cell from apoptosis by promoting the expression of bcl-2,reducing the expression of Bax and adjusting the ratio of Bcl-2/Bax,which would be one of the molecular mechanism of protective role in brain.

Key concepts: Apoptosis, Hypoxia (environmental), Brain damage, Ischemic preconditioning, Immunohistochemistry, BAX Protein, Hippocampus, Cell damage

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