2009Chinese Journal of Neuroimmunology and NeurologyRequires access

The Experimental Study on the Apoptosis of the Hippocampal CA1 Subregion after Focal Cerebral Ischemia Reperfusion in Rats

Lisha Chang

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Abstract

Objective To observe the neuronal apoptosis, the changes of tunel positive cells, the expression of Bcl-2, Bax proteins after local cerebral ischemia reperfusion in the hippocampal CA1 subregion of rats. Methods Healthy male SD (Sprague-Dawley) rats were used and were taken randomly into two groups: (1)SO (sham operation) group; (2)I/R(ischemia reperfusion) group. Then each group was taken into 3 h, 6 h, 12 h, 24 h, 48 h, 72 h subgroup according to the different reperfusion time, totally six groups. Bcl-2, Bax proteins and values of Bcl-2/Bax were checked by immunohistochemical staining methods in the hippocampal CA1 subregion. Apoptosis of cells was observed by TUNEL staining methods. Results There was little Bax expression in the contralateral hippocampal CA1 subregion which shows no ischemia in each group. In the ischemic hippocampal CA1 subregion of the I/R group, the expression of Bax was still little 3 hour after reperfusion. The expression of Bax began increasing 6 hour after reperfusion, it peaked at 24 h. The expression decreased significantly compared with that in I/R group, there were significant differences among these groups (P0. 05). Conclusions After cerebral reperfusion injury, there is not only denaturation and necrotic neurons, but also apoptosis. Maybe apoptosis was the main died style in the hippocampus CA1 subregion. Cerebral ischemia reperfusion can induce the expression of Bcl-2 and Bax. Cell apoptosis plays an important role in the cerebral ischemia reperfusion injury. The expression of Bcl-2 and Bax has some rule in hippocampal CAl neurons in focal cerebral ischemia reperfusion in rats.

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Objective To observe the neuronal apoptosis, the changes of tunel positive cells, the expression of Bcl-2, Bax proteins after local cerebral ischemia reperfusion in the hippocampal CA1 subregion of rats. Methods Healthy male SD (Sprague-Dawley) rats were used and were taken randomly into two groups: (1)SO (sham operation) group; (2)I/R(ischemia reperfusion) group. Then each group was taken into 3 h, 6 h, 12 h, 24 h, 48 h, 72 h subgroup according to the different reperfusion time, totally six groups. Bcl-2, Bax proteins and values of Bcl-2/Bax were checked by immunohistochemical staining methods in the hippocampal CA1 subregion. Apoptosis of cells was observed by TUNEL staining methods. Results There was little Bax expression in the contralateral hippocampal CA1 subregion which shows no ischemia in each group. In the ischemic hippocampal CA1 subregion of the I/R group, the expression of Bax was still little 3 hour after reperfusion. The expression of Bax began increasing 6 hour after reperfusion, it peaked at 24 h. The expression decreased significantly compared with that in I/R group, there were significant differences among these groups (P0. 05). Conclusions After cerebral reperfusion injury, there is not only denaturation and necrotic neurons, but also apoptosis. Maybe apoptosis was the main died style in the hippocampus CA1 subregion. Cerebral ischemia reperfusion can induce the expression of Bcl-2 and Bax. Cell apoptosis plays an important role in the cerebral ischemia reperfusion injury. The expression of Bcl-2 and Bax has some rule in hippocampal CAl neurons in focal cerebral ischemia reperfusion in rats.

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Available abstract

Objective To observe the neuronal apoptosis, the changes of tunel positive cells, the expression of Bcl-2, Bax proteins after local cerebral ischemia reperfusion in the hippocampal CA1 subregion of rats. Methods Healthy male SD (Sprague-Dawley) rats were used and were taken randomly into two groups: (1)SO (sham operation) group; (2)I/R(ischemia reperfusion) group. Then each group was taken into 3 h, 6 h, 12 h, 24 h, 48 h, 72 h subgroup according to the different reperfusion time, totally six groups. Bcl-2, Bax proteins and values of Bcl-2/Bax were checked by immunohistochemical staining methods in the hippocampal CA1 subregion. Apoptosis of cells was observed by TUNEL staining methods. Results There was little Bax expression in the contralateral hippocampal CA1 subregion which shows no ischemia in each group. In the ischemic hippocampal CA1 subregion of the I/R group, the expression of Bax was still little 3 hour after reperfusion. The expression of Bax began increasing 6 hour after reperfusion, it peaked at 24 h. The expression decreased significantly compared with that in I/R group, there were significant differences among these groups (P0. 05). Conclusions After cerebral reperfusion injury, there is not only denaturation and necrotic neurons, but also apoptosis. Maybe apoptosis was the main died style in the hippocampus CA1 subregion. Cerebral ischemia reperfusion can induce the expression of Bcl-2 and Bax. Cell apoptosis plays an important role in the cerebral ischemia reperfusion injury. The expression of Bcl-2 and Bax has some rule in hippocampal CAl neurons in focal cerebral ischemia reperfusion in rats.

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

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