急性癫痫大鼠海马Ca3区的Bcl-2、Caspase-3蛋白表达变化

目的探讨Bcl-2、Caspase-3在马桑内酯所致癫痫大鼠海马Ca3区的表达变化。方法40只SD大鼠随机分为癫痫组30只（又分为3h、6h、24h三个亚组）和对照组10只，应用免疫组织化学方法检测海马神经元中Bcl-2、Caspase-3的表达。结果①Bcl-2于致痫后6h表达增加，并于24h减少，与对照组比较有显著性差异（p〈0．05）。②Caspase-3于致痫后6h表达增加，并持续增加到24h，与对照组比较有显著性差异（p〈0．05）。③致痫组Bcl-2与Caspase-3的表达成反比，差异有统计学意义（p〈0．05）。结论Caspase-3蛋白的表达水平在癫痫发作后神经元的损伤中占有重要的作用，参与其凋亡的发生及其它功能的调控。Bcl-2可通过抑制Caspase-3的活性而抑制神经元的损伤，但是这种抑制作用是有限的。     

褪黑素对癫痫脑损伤神经保护作用的研究进展

癫痫是神经系统的常见病,病因复杂,痫性发作可改变脑内神经递质及其调质的释放,影响细胞跨膜信息的正常传递,使多种神经营养因子、神经肽的表达增强,导致神经细胞损伤。褪黑素(MLT)作为内源性神经内分泌激素,对中枢神经系统有直接和间接的生理调节作用,对睡眠障碍、抑郁症和精神疾病具有治疗作用,并对神经细胞有保护作用,也可对抗癫痫所致的自由基释放、氧化损伤等。因此,MLT对神经系统疾病特别是癫痫具有治疗作用。本文就MLT对癫痫脑损伤神经保护作用及其可能机制的研究进展进行综述。     

急性癫痫大鼠海马CA3区Bcl-2表达及线粒体改变

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.     

难治性癫痫发病机制研究进展

随着对难治性癫痫研究的不断深入,难治性癫痫发病机制理论方面的研究已经取得许多突破性进展,促进了临床进一步研究和诊断的准确性。本文就难治性癫痫的定义,发病机制的研究现状和尚待解决的问题进行综述,为抗癫痫药物的更新和非药物治疗手段的开展奠定基础。     

女性癫痫与生殖内分泌

癫痫是神经科常见的一种慢性脑部疾患，也是育龄期妇女的常见病，据统计，每200名妊娠妇女中就有1名癫痫患者。由于女性特殊的生殖内分泌特点和抗癫痫药物对女性妊娠、生育的影响，大约有40％的患者妊娠后癫痫发作更加频繁，且大量女性癫痫患者出现多囊肾、月经失调等生殖内分泌紊乱的表现，使得女性癫痫病人的治疗成为临床医生所关注的焦点。