癫痫发病率高，治愈率低，早期外源性给予低浓度H2S可抑制癫痫发作，高浓度则加剧其发作，然而低浓度H2S治疗癫痫的作用机制尚不清楚。本项目拟合成自身发光的BODIPY结构硫化氢供体探针，通过cck-8、细胞凋亡、激光共聚焦等检测探针的安全性，在细胞水平，建立海马神经元无镁细胞外液癫痫细胞模型，分析细胞周期变化，示踪光学探针在细胞的代谢情况，Western blot和RT-qPCR检测KATP通道mRNA和蛋白的表达，膜片钳记录神经元膜KATP通道电流及动作电位变化，探讨硫化氢供体探针对海马神经元间歇性放电抑制的分子作用机制；在动物水平，建立动物癫痫模型，侧脑室注射硫化氢探针外源性补充硫化氢，通过行为学观察、脑电及海马病理检测等方法筛选硫化氢治疗癫痫的最适浓度，并详细分析脑组织切片的上述分子生物学指标；深入探讨体内低浓度H2S调节KATP通道的分子作用机制，为癫痫的治疗提供理论基础。

As the high incidence of epilepsy,and low cure rate,early exogenous low concentration of H2S can effectively inhibit seizures, high concentrations increased their attacks, however, mechanism of the treatment of epilepsy by low concentration of H2S is still not clear.In this study, we firstly synthesize the hydrogen sulfide donor probe of BODIPY structure, detect the safety of the probe by CCK-8, apoptosis, laser confocal microscopy . At cell level, we culture the hippocampal neurons without magnesium to establish epilepsy cell model then to analyze the cell cycle changes and trace the metabolic status of optical probe,to determine the expression of KATP channel mRNA and protein by Western blot and RT-qPCR , and use the patch clamp to record the membrane KATP channel current and action potential changes in section of brain neuron. Then to investigate the molecular mechanism of hydrogen sulfide donor probe restrain intermittent firing of hippocampal neurons. At the animal level, we establish the epilepsy animal models,provide hydrogen sulfide exogenously by intracerebroventricular injection of hydrogen sulfide probe, then screen the optimal concentration of hydrogen sulfide in treatment of epilepsy through the behavior observation, EEG and hippocampal pathology detection method et al , further, analyzed in detail the molecular biological indexes of brain tissue slices,.and investigate the mechanism of low concentration of H2S in the regulation of KATP channels, then provide the theoretical basis for the treatment of epilepsy.