摘要： 目的  应用蛋白质芯片技术筛选海人酸致痫大鼠于α-细辛醚治疗前后海马区差异表达蛋白质，寻找α-细辛醚治疗癫痫的药物作用靶点。方法  健康成年SD 大鼠20 只，随机分为模型组和α-细辛醚组，经腹腔注射海人酸制备癫痫模型，选择Racine 发作标准达Ⅳ ~ Ⅴ级的大鼠作为观察动物，BCA法分别测量α-细辛醚治疗前后海马组织差异表达的蛋白质水平，以INR ≥ 1.30 表示蛋白质表达水平上调、INR ≤ 0.77 表示蛋白质表达水平下调。结果  共发现35 种差异表达的蛋白质，与模型组大鼠相比，α-细辛醚组大鼠海马组织共有5 种高表达蛋白质、30 种低表达蛋白质，其中大多数蛋白质参与了机体的细胞信号转导、细胞周期调控、基因转录及调控、细胞凋亡和神经生物学等重要生物功能。结论  α-细辛醚可调节由海人酸诱发的SD 大鼠海马组织中多种蛋白质的表达变化，提示α-细辛醚具有多个药物治疗靶点。

关键词: 石菖蒲； 细辛醚； 癫痫； 寡核苷酸探针； 蛋白质类； 疾病模型, 动物

Abstract: Objective To explore the effects of α-asarone on expressions of proteins in hippocampus of rats with seizures induced by kainic acid (KA), and find the drug action targets of α-asarone. Methods Twenty healthy male Sprague-Dawley (SD) rats were given KA by intraperitoneal injection to induce epilepsy, and were randomly divided into 2 groups: the KA group (n = 10) and α-asarone (24 mg/kg) group (n = 10). In α-asarone group α-asarone were administered once daily by intraperitoneal injection in 7 consecutive days. Bicinchoninic acid (BCA) method was used to measure the protein expression in hippocampus before and after α-asarone therapy. The endogenous international normalized ratio (INR) was calculated according to the standardization of hybridization fluorescence signal strength, and was used to measure the difference of protein expression between the two groups. INR ≥ 1.30 indicated the protein expression up-regulated while INR ≤ 0.77 indicated the protein expression down-regulated. Results Thirty-five differentially expressed proteins were found. In comparison with KA group 5 proteins presented higher expression, while 30 lower expression in α-asarone group, and most of them involved in signal transduction, cell cycle regulation, gene transcription and regulation, apoptosis, and neurobiological functions. Conclusion α-Asarone may regulate a variety of protein expression in hippocampus of rats with seizures induced by kainic acid, and it may indicate that the drug has multiple therapeutic targets.

Key words: Acorus tatarinowii, Asarone, Epilepsy, Oligonucleotide probes, Proteins, Disease models, animal