摘要
BACKGROUND： Previous studies have shown that the mitochondrial structure and function are damaged in animal models of epilepsy. In addition, the Bcl-2 protein is capable of regulating mitochondrial stability. OBJECTIVE： To observe and validate changes in mitochondrial structure and Bcl-2 expression, and to analyze these characteristics in the hippocampal CA3 region of rat models of epilepsy. DESIGN, TIME AND SETTING： This randomized, controlled, animal experiment was performed at the Laboratory of Electron Microscopy and Department of Histology and Embryology, Luzhou Medical College between 2007 and 2008. MATERIALS： Coriamyrtin was provided by the Pharmacy Factory of West China University of Medical Sciences. The primary and secondary antibodies were provided by Zhongshan Goldenbridge Biotechnology, Beijing. METHODS： A total of 44 adult, male, Sprague Dawley rats were randomly divided into control （n = 11） and epilepsy （n = 33） groups. Rats in the epilepsy group were induced by coriamyrtin （50 μ g/kg）, which was injected into the lateral ventricles. The rats were then observed at 3, 6, and 24 hours after epilepsy induction, with 11 rats at each time point. Epilepsy was not induced in rats from the control group. MAIN OUTCOME MEASURES： Pathological changes in the hippocampal CA3 region were observed by light microscopy; Bcl-2 expression was analyzed by immunohistochemistry; and mitochondrial changes in the hippocampus were observed under transmission electron microscopy. RESULTS： （1） The control group displayed very little Bcl-2 protein expression in the hippocampal CA3 region. However, after 3 hours of epilepsy, expression was visible. By 6 hours, expression peaked and then subsequently decreased after 24 hours, but remained higher than the control group （P 〈 0.05）. （2） Mitochondria were damaged to varying degrees in the epilepsy groups. For example, mitochondria edema, cristae space increase, and disappearance of mitochondria were apparent. Moreover, mitochondrial damage occurred prior to pathological changes in the neurons and nucleolus. CONCLUSION： Bcl-2 expression and mitochondrial damage increased in the hippocampal CA3 region in rats with epilepsy. Moreover, mitochondrial damage occurred prior to increased Bcl-2 expression and nucleolus damage.
BACKGROUND： Previous studies have shown that the mitochondrial structure and function are damaged in animal models of epilepsy. In addition, the Bcl-2 protein is capable of regulating mitochondrial stability. OBJECTIVE： To observe and validate changes in mitochondrial structure and Bcl-2 expression, and to analyze these characteristics in the hippocampal CA3 region of rat models of epilepsy. DESIGN, TIME AND SETTING： This randomized, controlled, animal experiment was performed at the Laboratory of Electron Microscopy and Department of Histology and Embryology, Luzhou Medical College between 2007 and 2008. MATERIALS： Coriamyrtin was provided by the Pharmacy Factory of West China University of Medical Sciences. The primary and secondary antibodies were provided by Zhongshan Goldenbridge Biotechnology, Beijing. METHODS： A total of 44 adult, male, Sprague Dawley rats were randomly divided into control （n = 11） and epilepsy （n = 33） groups. Rats in the epilepsy group were induced by coriamyrtin （50 μ g/kg）, which was injected into the lateral ventricles. The rats were then observed at 3, 6, and 24 hours after epilepsy induction, with 11 rats at each time point. Epilepsy was not induced in rats from the control group. MAIN OUTCOME MEASURES： Pathological changes in the hippocampal CA3 region were observed by light microscopy; Bcl-2 expression was analyzed by immunohistochemistry; and mitochondrial changes in the hippocampus were observed under transmission electron microscopy. RESULTS： （1） The control group displayed very little Bcl-2 protein expression in the hippocampal CA3 region. However, after 3 hours of epilepsy, expression was visible. By 6 hours, expression peaked and then subsequently decreased after 24 hours, but remained higher than the control group （P 〈 0.05）. （2） Mitochondria were damaged to varying degrees in the epilepsy groups. For example, mitochondria edema, cristae space increase, and disappearance of mitochondria were apparent. Moreover, mitochondrial damage occurred prior to pathological changes in the neurons and nucleolus. CONCLUSION： Bcl-2 expression and mitochondrial damage increased in the hippocampal CA3 region in rats with epilepsy. Moreover, mitochondrial damage occurred prior to increased Bcl-2 expression and nucleolus damage.
基金
Supported by:the Foundation of Sichuan Bureau of Science and Technology,No. 05JY029-103
the Foundation of Sichuan Educational Bureau,No. 149-01LA40:2005B013
