2009Inner Mongolia Medical JournalRequires access

The Effect of Nimodipine on The Neuron Apoptosis Following Focal Cerebral Ischemia-reperfusion on Middle Cerebral Artery in Rats

Lirong Zhang

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Abstract

Objective:To investigate the neuron apoptosis in the MCAO rat models of focal cerebral ischemia-reperfusion and the effect of nimodipine on them.Methods: 120 male Wistar rate weighing 250~300 g were randomly divided into four groups,normal group,sham operation group,cerebral ischemic group and nimodipine-applied group.Cerebral ischemic and nimodipine-applied groups were further divided into 1、3、6、12、24、36、48、72 hour and 7 days groups according to the time of reperfusion after cerebral ischemia respectively.Focal cerebral ischemic rat models were subjected to right middle cerebral artery occlusion(RMCAO)by a suture lasting for 2 hours and followed by reperfusion.Then record the neurologic impairment of these rats.Apoptosis was analyzed by TdT mediated dUTP-biotin nick end labeling using light microscope and image analysis system.Results: The number of apoptosis positive cells in cerebral ischemic group at different time point were higher compared with sham operation and normal groups (P0.05).The number of apoptosim positive cells were decreased after using nimodipine(P0.05).Conclusion: Nimedipine might inhibit the development of neuron apoptosis in rats after ischemia and reperfusion and have the neuroprotective effect against ischemia and reperfusion injury.

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Objective:To investigate the neuron apoptosis in the MCAO rat models of focal cerebral ischemia-reperfusion and the effect of nimodipine on them.Methods: 120 male Wistar rate weighing 250~300 g were randomly divided into four groups,normal group,sham operation group,cerebral ischemic group and nimodipine-applied group.Cerebral ischemic and nimodipine-applied groups were further divided into 1、3、6、12、24、36、48、72 hour and 7 days groups according to the time of reperfusion after cerebral ischemia respectively.Focal cerebral ischemic rat models were subjected to right middle cerebral artery occlusion(RMCAO)by a suture lasting for 2 hours and followed by reperfusion.Then record the neurologic impairment of these rats.Apoptosis was analyzed by TdT mediated dUTP-biotin nick end labeling using light microscope and image analysis system.Results: The number of apoptosis positive cells in cerebral ischemic group at different time point were higher compared with sham operation and normal groups (P0.05).The number of apoptosim positive cells were decreased after using nimodipine(P0.05).Conclusion: Nimedipine might inhibit the development of neuron apoptosis in rats after ischemia and reperfusion and have the neuroprotective effect against ischemia and reperfusion injury.

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Available abstract

Objective:To investigate the neuron apoptosis in the MCAO rat models of focal cerebral ischemia-reperfusion and the effect of nimodipine on them.Methods: 120 male Wistar rate weighing 250~300 g were randomly divided into four groups,normal group,sham operation group,cerebral ischemic group and nimodipine-applied group.Cerebral ischemic and nimodipine-applied groups were further divided into 1、3、6、12、24、36、48、72 hour and 7 days groups according to the time of reperfusion after cerebral ischemia respectively.Focal cerebral ischemic rat models were subjected to right middle cerebral artery occlusion(RMCAO)by a suture lasting for 2 hours and followed by reperfusion.Then record the neurologic impairment of these rats.Apoptosis was analyzed by TdT mediated dUTP-biotin nick end labeling using light microscope and image analysis system.Results: The number of apoptosis positive cells in cerebral ischemic group at different time point were higher compared with sham operation and normal groups (P0.05).The number of apoptosim positive cells were decreased after using nimodipine(P0.05).Conclusion: Nimedipine might inhibit the development of neuron apoptosis in rats after ischemia and reperfusion and have the neuroprotective effect against ischemia and reperfusion injury.

Key concepts: Nimodipine, Medicine, Ischemia, Neuroprotection, Middle cerebral artery, Anesthesia, Apoptosis, Reperfusion injury

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