癫痫,一种慢性神经系统疾病,其特征是反复发作的无缘无故的癫痫发作,在大约三分之一表现出对常规药物治疗的抗性的病例中提出了实质性挑战。这项研究调查了4-烯丙基-2,6-二甲氧基苯酚的作用,来自各种天然来源的酚类化合物,在不同的诱发癫痫发作模型及其对动物脑电图(EEG)记录的影响。用4-烯丙基-2,6-二甲氧基苯酚(50、100或200mg/kg)的剂量曲线对成年雄性瑞士白化病小鼠进行预处理(i.p.),它的车辆(吐温),或标准抗癫痫药(地西泮或苯妥英)。随后,对小鼠进行不同的癫痫发作诱导模型-戊四唑(PTZ),3-巯基丙酸(3-MPA),毛果芸香碱(PILO),或最大电击发作(MES)。对手术植入电极的其他动物进行EEG分析以评估脑活动。重要结果表明,用4-烯丙基-2,6-二甲氧基苯酚治疗的动物在PTZ和PILO模型中表现出第一次肌阵挛性发作的潜伏期增加;PTZ中第一次强直阵挛性发作的潜伏期延长,3-MPA,和PILO模型;PTZ和PILO模型中强直阵挛性癫痫发作的总持续时间减少;PTZ和3-MPA模型中惊厥性癫痫发作的强度降低;3-MPA中的死亡率降低,PILO,和MES模型。EEG分析表明,给予4-烯丙基-2,6-二甲氧基苯酚后,归因于β波的总功率百分比增加。值得注意的是,在PTZ模型中保护免受行为和电子图癫痫发作的物质,防止记录信号的平均幅度增加,同时也引起θ波和伽马波的参与增加。这些发现表明,在不同的临床前癫痫发作模型中,所测试的酚类化合物的有希望的结果。强调需要进一步的全面研究来阐明其潜在机制并验证其在癫痫治疗中的临床相关性。
Epilepsy, a chronic neurological disorder characterized by recurrent unprovoked seizures, presents a substantial challenge in approximately one-third of cases exhibiting resistance to conventional pharmacological treatments. This study investigated the effect of 4-allyl-2,6-dimethoxyphenol, a phenolic compound derived from various natural sources, in different models of induced seizures and its impact on animal electroencephalographic (EEG) recordings. Adult male Swiss albino mice were pre-treated (i.p.) with a dose curve of 4-allyl-2,6-dimethoxyphenol (50, 100, or 200 mg/kg), its vehicle (Tween), or standard antiepileptic drug (Diazepam; or Phenytoin). Subsequently, the mice were subjected to different seizure-inducing models - pentylenetetrazole (PTZ), 3-mercaptopropionic acid (3-MPA), pilocarpine (PILO), or maximal electroshock seizure (MES). EEG analysis was performed on other animals surgically implanted with electrodes to evaluate brain activity. Significant results revealed that animals treated with 4-allyl-2,6-dimethoxyphenol exhibited increased latency to the first myoclonic jerk in the PTZ and PILO models; prolonged latency to the first tonic-clonic seizure in the PTZ, 3-MPA, and PILO models; reduced total duration of tonic-clonic seizures in the PTZ and PILO models; decreased intensity of convulsive seizures in the PTZ and 3-MPA models; and diminished mortality in the 3-MPA, PILO, and MES models. EEG analysis indicated an increase in the percentage of total power attributed to beta waves following 4-allyl-2,6-dimethoxyphenol administration. Notably, the substance protected from behavioral and electrographic seizures in the PTZ model, preventing increases in the average amplitude of recording signals while also inducing an increase in the participation of theta and gamma waves. These findings suggest promising outcomes for the tested phenolic compound across diverse pre-clinical seizure models, highlighting the need for further comprehensive studies to elucidate its underlying mechanisms and validate its clinical relevance in epilepsy management.