CAJ | 학술논문

目的观察阿曼托双黄酮(AF)对匹罗卡品点燃小鼠癫痫发作、海马神经元的影响,并探讨其机制.方法建立匹罗卡品小鼠点燃模型,并给予AF进行干预.综合应用神经电生理、病理学、分子生物学等技术,观察AF对点燃小鼠癫痫发作以及海马神经元的影响.结果与癫痫组比较,AF组小鼠行为学和局部场电位信号(LFP)表现均相对稳定,海马CA1区存活神经元数目显著增加[(121.40 ±8.72)个,P＜0.05],原位末端转移酶标记(TUNEL)染色结果显示凋亡神经元数目减少[(1.70±0.98)个,P＜0.01],免疫组织化学(4 894.25±771.18)和Western blot结果(0.49±0.13)显示核因子-κB(NF-κB) p65表达明显降低(P＜0.01).结论 AF对小鼠癫痫模型具有明显的预防惊厥发生和神经保护作用,其作用机制与AF抑制癫痫发生时的脑内炎性反应有关.
목적 관찰아만탁쌍황동(AF)대필라잡품점연소서전간발작、해마신경원적영향,병탐토기궤제.방법 건립필라잡품소서점연모형,병급여AF진행간예.종합응용신경전생리、병이학、분자생물학등기술,관찰AF대점연소서전간발작이급해마신경원적영향.결과 여전간조비교,AF조소서행위학화국부장전위신호(LFP)표현균상대은정,해마CA1구존활신경원수목현저증가[(121.40 ±8.72)개,P＜0.05],원위말단전이매표기(TUNEL)염색결과현시조망신경원수목감소[(1.70±0.98)개,P＜0.01],면역조직화학(4 894.25±771.18)화Western blot결과(0.49±0.13)현시핵인자-κB(NF-κB) p65표체명현강저(P＜0.01).결론 AF대소서전간모형구유명현적예방량궐발생화신경보호작용,기작용궤제여AF억제전간발생시적뇌내염성반응유관.
Objective To study the effect of amentoflavone on seizures and hippocampal neurons in the model of kindling mice induced by pilocarpine,and to explore the mechanism.Methods A kindling model of pilocarpine-induced epilepsy in mice was established,and intervened with amentoflavone.The techniques of neuroelectrophysiology,pathology and molecular biology were used to analyze the influence of amentoflavone on kindling mice and the protective effect on hippocampal neurons.Results The behaviors and electroencephalogram (EEG) of mice in AF group were stable.As compared with epilepsy group,the number of hippocampal CA1 neurons survived was significantly increased (121.40 ± 8.72 vs.1.70 ± 0.98,P ＜0.05),the number of apoptotic neurons with TdT-mediated dUTP nick end labeling (TUNEL) staining was reduced (P ＜ 0.01),and the expression of nuclear factor-κB p65 was significantly decreased in AF group (immunohistochemistry:4 894.25 ± 771.18; Western blotting:0.49 ± 0.13,P ＜ 0.01).Conclusion Amentoflavone exerts a significant preventive effect on seizures and neuroprotection in the hippocampus,and its mechanisms is related to the inhibitory effect of amentoflavone on inflammatory response of brain in epilepsy process.