2004Acta Academiae Medicinae XuzhouRequires access

The expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its significance

Hong Cao

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Abstract

ObjectiveTo investigate t he expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its effects. MethodsGerbils were randomly divided into sham group (SH), ischemic-preconditi oning control group (IC), ischemic-preconditioning test group (IP) and ischemia- reperfusion (without preconditioning) group (IR). Forebrain ischemia was induced by occlusion of bilateral common carotid arteries. Observations were carried ou t in each group 1 d, 3 d, 5 d and 7 d after ischemia: open field test was used t o examine the behavioral change, the apoptosis neurons in hippocampal CA1 region was counted, the expression of Bcl-2 and Bax in hippocampal CA1 area was detect ed by SABC immunocytochemical technique. ResultsThe beha vioral mark and the number of apoptosis neurons in hippocampal CA1 region were m uch less in IP group than in IR group (P0.01). The expression of Bcl-2 was more and the expression of Bax was less in CA1 area in IP group than in IR grou p (P0.01). ConclusionIschemic preconditioning can significantly protect neurons against cerebral ischemia, and modulating the expr ession of apoptosis related genes Bcl-2 and Bax may be one of the protective me chanisms.

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ObjectiveTo investigate t he expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its effects. MethodsGerbils were randomly divided into sham group (SH), ischemic-preconditi oning control group (IC), ischemic-preconditioning test group (IP) and ischemia- reperfusion (without preconditioning) group (IR). Forebrain ischemia was induced by occlusion of bilateral common carotid arteries. Observations were carried ou t in each group 1 d, 3 d, 5 d and 7 d after ischemia: open field test was used t o examine the behavioral change, the apoptosis neurons in hippocampal CA1 region was counted, the expression of Bcl-2 and Bax in hippocampal CA1 area was detect ed by SABC immunocytochemical technique. ResultsThe beha vioral mark and the number of apoptosis neurons in hippocampal CA1 region were m uch less in IP group than in IR group (P0.01). The expression of Bcl-2 was more and the expression of Bax was less in CA1 area in IP group than in IR grou p (P0.01). ConclusionIschemic preconditioning can significantly protect neurons against cerebral ischemia, and modulating the expr ession of apoptosis related genes Bcl-2 and Bax may be one of the protective me chanisms.

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Available abstract

ObjectiveTo investigate t he expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its effects. MethodsGerbils were randomly divided into sham group (SH), ischemic-preconditi oning control group (IC), ischemic-preconditioning test group (IP) and ischemia- reperfusion (without preconditioning) group (IR). Forebrain ischemia was induced by occlusion of bilateral common carotid arteries. Observations were carried ou t in each group 1 d, 3 d, 5 d and 7 d after ischemia: open field test was used t o examine the behavioral change, the apoptosis neurons in hippocampal CA1 region was counted, the expression of Bcl-2 and Bax in hippocampal CA1 area was detect ed by SABC immunocytochemical technique. ResultsThe beha vioral mark and the number of apoptosis neurons in hippocampal CA1 region were m uch less in IP group than in IR group (P0.01). The expression of Bcl-2 was more and the expression of Bax was less in CA1 area in IP group than in IR grou p (P0.01). ConclusionIschemic preconditioning can significantly protect neurons against cerebral ischemia, and modulating the expr ession of apoptosis related genes Bcl-2 and Bax may be one of the protective me chanisms.

Key concepts: Hippocampal formation, Ischemic preconditioning, Apoptosis, Ischemia, Hippocampus, Occlusion, Anesthesia, Neuroscience

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