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Mitochondrial damage in hippocampal neurons of rats with epileptic protein expression of Fas and caspase-3

机译:癫痫发作毒性蛋白表达的大鼠海马神经元的线粒体损伤

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Epilepsy model in rats was established to observe the behavior and pathological changes, and to detect mitochondrial dysfunction, exploring its possible molecular mechanisms. The epileptic status of Sprague-Dawley (SD) rats was induced by intraperitoneal injection of lithium chloride, and the change of behavior was recorded. Electroencephalogram (EEG) was used to measure the abnormal discharge of neurons in rats. The brain tissue was fixed with polyformaldehyde and the paraffin sections were prepared, and the damage of the hippocampal neurons was observed with Nissl staining. Mitochondrial ATP and mitochondrial DNA were examined to assess mitochondrial dysfunction. Finally, qPCR and western blot analysis were used to detect mRNA and protein expression of fatty acid synthetase (Fas), Fas ligand (FasL) and caspase-3 in rat hippocampal neurons. The correlation between the mitochondrial dysfunction of rat hippocampal neurons and Fas and caspase-3 was analyzed. Compared with the normal group rats, the model group showed typical seizures, which were determined by the Racine attack score. EEG of the hippocampus of the model group was recorded in cluster in model group rats. Nissl staining showed a different degree of damage to the hippocampal neurons in the model group compared with normal rats. The mitochondrial ATP content and DNA content of rat hippocampal neurons in the model group were significantly lower than that of normal rats (P<0.01). The qPCR and western blot results showed that the mRNA and protein expression levels of Fas, FasL and caspase-3 were significantly increased in the hippocampus of rat model group (P<0.01). The expression level of Fas and caspase-3 in hippocampal tissues of rats was negatively correlated with mitochondrial DNA content. In conclusion, seizures cause damage of neuron mitochondria in rat hippocampus leading to death of hippocampal neurons, the mitochondrial damage of hippocampal neurons in epileptic rats was closely related to the expression of Fas and caspase-3.
机译:成立了大鼠的癫痫模型,观察到行为和病理变化,并检测线粒体功能障碍,探索其可能的分子机制。通过腹膜内注射氯化锂诱导Sprague-Dawley(SD)大鼠的癫痫状态,并记录了行为的变化。脑电图(EEG)用于测量大鼠神经元的异常放电。将脑组织用聚异体醛固定,并制备石蜡切片,并用NISSL染色观察海马神经元的损伤。检查线粒体ATP和线粒体DNA以评估线粒体功能障碍。最后,使用QPCR和Western印迹分析来检测脂肪酸合成酶(FAS),Fas配体(FasL)和Caspase-3的mRNA和蛋白表达在大鼠海马神经元中。分析了大鼠海马神经元和Fas和Caspase-3的线粒体功能障碍之间的相关性。与正常群体大鼠相比,模型组显示典型的癫痫发作,由RACINE攻击分数决定。模型组的海马的脑电图被记录在模型组大鼠中的群中。与正常大鼠相比,Nissl染色对模型组中的海马神经元造成不同程度的损伤。模型组中大鼠海马神经元的线粒体ATP含量和DNA含量显着低于正常大鼠(P <0.01)。 QPCR和Western印迹结果表明,大鼠模型组海马的Fas,FasL和Caspase-3的mRNA和蛋白表达水平显着增加(P <0.01)。大鼠海马组织中FAS和Caspase-3的表达水平与线粒体DNA含量负相关。总之,癫痫发作导致大鼠海马的神经元线粒体损伤导致海马神经元死亡,癫痫大鼠海马神经元的线粒体损伤与Fas和Caspase-3的表达密切相关。

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