2008Unpublished venueRequires access

Effect of Nimodipine on apoptosis in hippocampal region of rats with cerebral ischemia-reperfusion injury

Chang-bai Bi, Hui Sun, Li-jin Xu

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Abstract

Objective To observe the protective effect of Nimodipine on the neurons of rats with global cerebral ischemia-reperfusion injury.Methods All rats were divided into three groups at random:sham-operated group,control group and treated group.Four-vessel occlusion was used to establish the model of global cerebral ischemia-reperfusion in the control group and treated group.The normal saline and Nimodipine was injected intraperitoneally in control groups and treated groups at 0?h,6?h,12?h,24?h after reperfusion respectively.The flow cytometry was used to determine cellular apoptosis rate and expression of Bcl-2、Bax protein.Results (1) The cellular apoptosis rate of hippocampal region in control group was higher than that in sham-operated group (P<0.01) and treated group (P<0.01).The cellular apoptosis rate was increased at 0?h and 6?h than 12?h and 24?h in treated group (P<0.05).The expression of Bcl-2 in treated group was higher than that in control group,while the expression of Bax in treated group was lower than that in control group.Conclusion Nimodipine could effectively reduce apoptosis after global cerebral ischemia-reperfusion injury.The mechanism of effects of Nimodipine would be related with increasing expression of Bcl-2.The effect would be better if useing it in earlier time-spot. Key words: Cerebral ischemia-reperfusion injury; Apoptosis; Bcl-2/ Bax; Nimodipine; Rat

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Objective To observe the protective effect of Nimodipine on the neurons of rats with global cerebral ischemia-reperfusion injury.Methods All rats were divided into three groups at random:sham-operated group,control group and treated group.Four-vessel occlusion was used to establish the model of global cerebral ischemia-reperfusion in the control group and treated group.The normal saline and Nimodipine was injected intraperitoneally in control groups and treated groups at 0?h,6?h,12?h,24?h after reperfusion respectively.The flow cytometry was used to determine cellular apoptosis rate and expression of Bcl-2、Bax protein.Results (1) The cellular apoptosis rate of hippocampal region in control group was higher than that in sham-operated group (P<0.01) and treated group (P<0.01).The cellular apoptosis rate was increased at 0?h and 6?h than 12?h and 24?h in treated group (P<0.05).The expression of Bcl-2 in treated group was higher than that in control group,while the expression of Bax in treated group was lower than that in control group.Conclusion Nimodipine could effectively reduce apoptosis after global cerebral ischemia-reperfusion injury.The mechanism of effects of Nimodipine would be related with increasing expression of Bcl-2.The effect would be better if useing it in earlier time-spot. Key words: Cerebral ischemia-reperfusion injury; Apoptosis; Bcl-2/ Bax; Nimodipine; Rat

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Available abstract

Objective To observe the protective effect of Nimodipine on the neurons of rats with global cerebral ischemia-reperfusion injury.Methods All rats were divided into three groups at random:sham-operated group,control group and treated group.Four-vessel occlusion was used to establish the model of global cerebral ischemia-reperfusion in the control group and treated group.The normal saline and Nimodipine was injected intraperitoneally in control groups and treated groups at 0?h,6?h,12?h,24?h after reperfusion respectively.The flow cytometry was used to determine cellular apoptosis rate and expression of Bcl-2、Bax protein.Results (1) The cellular apoptosis rate of hippocampal region in control group was higher than that in sham-operated group (P<0.01) and treated group (P<0.01).The cellular apoptosis rate was increased at 0?h and 6?h than 12?h and 24?h in treated group (P<0.05).The expression of Bcl-2 in treated group was higher than that in control group,while the expression of Bax in treated group was lower than that in control group.Conclusion Nimodipine could effectively reduce apoptosis after global cerebral ischemia-reperfusion injury.The mechanism of effects of Nimodipine would be related with increasing expression of Bcl-2.The effect would be better if useing it in earlier time-spot. Key words: Cerebral ischemia-reperfusion injury; Apoptosis; Bcl-2/ Bax; Nimodipine; Rat

Key concepts: Nimodipine, Medicine, Apoptosis, Ischemia, Hippocampal formation, Reperfusion injury, Anesthesia, Saline

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