2013Journal of Nanchang UniversityRequires access

Effects of Protectin D1 on Hippocampal Caspase-3 Expression and Neuronal Apoptosis following Global Cerebral Ischemia-Reperfusion in Rats

Qiaoyu Li

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Abstract

Objective To investigate the effects of protectin D1( PD1) on the expression of hippocampal caspase-3 and neuronal apoptosis following global cerebral ischemia-reperfusion( I / R) in rats.Methods One hundred and eight healthy male Sprague-Dawley rats were randomly divided into three groups: sham operation group( group S),global cerebral I / R group( group IR) and PD1 group( group P),with 36 rats in each group. Global cerebral I / R was produced by 4-vessel occlusion technique. In group P,PD1( 100 ng) was injected into cerebral ventricles at the moment of reperfusion. In group S and group IR,rats were given the same volume of normal saline. Six rats in each group were killed after 2,6,12,24,48 and 72 hours of reperfusion( T1-T6),respectively. Hippocampal tissues were obtained to detect the expression of caspase-3 protein and mRNA using Western blot and RT-PCR,respectively. Neuronal apoptosis was determined by flow cytometry. Results Compared with group S,the expression of hippocampal caspase-3 protein and mRNA significantly increased in group IR and group P( P 0. 05). Compared with group IR,the expression of hippocampal caspase-3 protein and mRNA significantly decreased in group P( P 0. 05). No neuronal apoptosis was found in group S at all time points. In group IR and group P,neuronal apoptosis rate began to increase at T1,reached the peak at T4,and began to decrease at T5. Compared with group IR,the apoptosis rate significantly decreased in group P at each time point( P 0. 05). Conclusion PD1 can inhibit hippocampal neuronal apoptosis induced by global cerebral I / R through down-regulation of caspase-3 protein and mRNA expression.

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Objective To investigate the effects of protectin D1( PD1) on the expression of hippocampal caspase-3 and neuronal apoptosis following global cerebral ischemia-reperfusion( I / R) in rats.Methods One hundred and eight healthy male Sprague-Dawley rats were randomly divided into three groups: sham operation group( group S),global cerebral I / R group( group IR) and PD1 group( group P),with 36 rats in each group. Global cerebral I / R was produced by 4-vessel occlusion technique. In group P,PD1( 100 ng) was injected into cerebral ventricles at the moment of reperfusion. In group S and group IR,rats were given the same volume of normal saline. Six rats in each group were killed after 2,6,12,24,48 and 72 hours of reperfusion( T1-T6),respectively. Hippocampal tissues were obtained to detect the expression of caspase-3 protein and mRNA using Western blot and RT-PCR,respectively. Neuronal apoptosis was determined by flow cytometry. Results Compared with group S,the expression of hippocampal caspase-3 protein and mRNA significantly increased in group IR and group P( P 0. 05). Compared with group IR,the expression of hippocampal caspase-3 protein and mRNA significantly decreased in group P( P 0. 05). No neuronal apoptosis was found in group S at all time points. In group IR and group P,neuronal apoptosis rate began to increase at T1,reached the peak at T4,and began to decrease at T5. Compared with group IR,the apoptosis rate significantly decreased in group P at each time point( P 0. 05). Conclusion PD1 can inhibit hippocampal neuronal apoptosis induced by global cerebral I / R through down-regulation of caspase-3 protein and mRNA expression.

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Available abstract

Objective To investigate the effects of protectin D1( PD1) on the expression of hippocampal caspase-3 and neuronal apoptosis following global cerebral ischemia-reperfusion( I / R) in rats.Methods One hundred and eight healthy male Sprague-Dawley rats were randomly divided into three groups: sham operation group( group S),global cerebral I / R group( group IR) and PD1 group( group P),with 36 rats in each group. Global cerebral I / R was produced by 4-vessel occlusion technique. In group P,PD1( 100 ng) was injected into cerebral ventricles at the moment of reperfusion. In group S and group IR,rats were given the same volume of normal saline. Six rats in each group were killed after 2,6,12,24,48 and 72 hours of reperfusion( T1-T6),respectively. Hippocampal tissues were obtained to detect the expression of caspase-3 protein and mRNA using Western blot and RT-PCR,respectively. Neuronal apoptosis was determined by flow cytometry. Results Compared with group S,the expression of hippocampal caspase-3 protein and mRNA significantly increased in group IR and group P( P 0. 05). Compared with group IR,the expression of hippocampal caspase-3 protein and mRNA significantly decreased in group P( P 0. 05). No neuronal apoptosis was found in group S at all time points. In group IR and group P,neuronal apoptosis rate began to increase at T1,reached the peak at T4,and began to decrease at T5. Compared with group IR,the apoptosis rate significantly decreased in group P at each time point( P 0. 05). Conclusion PD1 can inhibit hippocampal neuronal apoptosis induced by global cerebral I / R through down-regulation of caspase-3 protein and mRNA expression.

Key concepts: Hippocampal formation, Apoptosis, Ischemia, Western blot, Endocrinology, Internal medicine, Hippocampus, Caspase 3

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Effects of Protectin D1 on Hippocampal Caspase-3 Expression and Neuronal Apoptosis following Global Cerebral Ischemia-Reperfusion in Rats — Research Paper | ScholarLens