Department of Nutrition Science, Science and Research Branch, Faculty of Medical Science and Technology, Islamic Azad University, Shodada Hesarak Blvd, Tehran 1477893855, Iran.
Network of Interdisciplinarity in Neonates and Infants (NINI), Universal Scientific Education and Research Network (USERN), Dr. Qarib St, Tehran 1419733151, Iran.
Rev Neurosci. 2024 Feb 14;35(4):473-488. doi: 10.1515/revneuro-2023-0128. Print 2024 Jun 25.
Childhood epilepsy affects up to 1 % of children. It has been shown that 30 % of patients are resistant to drug treatments, making further investigation of other potential treatment strategies necessary. One such approach is the ketogenic diet (KD) showing promising results and potential benefits beyond the use of current antiepileptic drugs. This study aims to investigate the effects of KD on inflammation and oxidative stress, as one of the main suggested mechanisms of neuroprotection, in children with epilepsy. This narrative review was conducted using the Medline and Google Scholar databases, and by searching epilepsy, drug-resistant epilepsy, child, children, ketogenic, ketogenic diet, diet, ketogenic, keto, ketone bodies (BHB), PUFA, gut microbiota, inflammation, inflammation mediators, neurogenic inflammation, neuroinflammation, inflammatory marker, adenosine modulation, mitochondrial function, MTOR pathway, Nrf2 pathway, mitochondrial dysfunction, PPARɣ, oxidative stress, ROS/RNS, and stress oxidative as keywords. Compelling evidence underscores inflammation and oxidative stress as pivotal factors in epilepsy, even in cases with genetic origins. The ketogenic diet effectively addresses these factors by reducing ROS and RNS, enhancing antioxidant defenses, improving mitochondrial function, and regulating inflammatory genes. Additionally, KD curbs pro-inflammatory cytokine and chemokine production by dampening NF-κB activation, inhibiting the NLRP3 inflammasome, increasing brain adenosine levels, mTOR pathway inhibition, upregulating PPARɣ expression, and promoting a healthy gut microbiota while emphasizing the consumption of healthy fats. KD could be considered a promising therapeutic intervention in patients with epilepsy particularly in drug-resistant epilepsy cases, due to its targeted approach addressing oxidative stress and inflammatory mechanisms.
儿童癫痫影响高达 1%的儿童。已经表明，30%的患者对药物治疗有抗药性，因此有必要进一步研究其他潜在的治疗策略。酮饮食（KD）就是一种方法，它在超越目前抗癫痫药物的使用方面显示出有希望的结果和潜在的益处。本研究旨在调查 KD 对炎症和氧化应激的影响，这是神经保护的主要建议机制之一，在癫痫患儿中。本叙述性综述使用 Medline 和 Google Scholar 数据库进行，并通过搜索癫痫、耐药性癫痫、儿童、儿童、酮、酮饮食、饮食、酮、酮体（BHB）、PUFA、肠道微生物群、炎症、炎症介质、神经原性炎症、神经炎症、炎症标志物、腺苷调节、线粒体功能、MTOR 途径、Nrf2 途径、线粒体功能障碍、PPARɣ、氧化应激、ROS/RNS 和应激氧化作为关键字。有力的证据强调炎症和氧化应激是癫痫的关键因素，即使在有遗传起源的情况下也是如此。KD 通过减少 ROS 和 RNS、增强抗氧化防御、改善线粒体功能和调节炎症基因来有效解决这些因素。此外，KD 通过抑制 NF-κB 激活、抑制 NLRP3 炎性体、增加大脑腺苷水平、抑制 mTOR 途径、上调 PPARɣ 表达、促进健康的肠道微生物群来抑制促炎细胞因子和趋化因子的产生，同时强调健康脂肪的摄入。由于 KD 针对氧化应激和炎症机制的靶向治疗方法，因此可以被认为是癫痫患者，特别是耐药性癫痫患者的一种有前途的治疗干预措施。
