儿童癫痫影响多达1%的儿童。研究表明,30%的患者对药物治疗有抗药性,需要进一步调查其他潜在的治疗策略。一种这样的方法是生酮饮食(KD),显示出超出使用当前抗癫痫药物的有希望的结果和潜在益处。本研究旨在探讨KD对炎症和氧化应激的影响,作为神经保护的主要机制之一,癫痫儿童。这篇叙述性综述是使用Medline和GoogleScholar数据库进行的,通过搜索癫痫,耐药癫痫,孩子,孩子们,生酮,生酮饮食,饮食,生酮,keto,酮体(BHB),PUFA,肠道菌群,炎症,炎症介质,神经源性炎症,神经炎症,炎症标志物,腺苷调制,线粒体功能,MTOR通路,Nrf2通路,线粒体功能障碍,PPAR,氧化应激,ROS/RNS,和压力氧化作为关键词。令人信服的证据强调炎症和氧化应激是癫痫的关键因素,即使是遗传起源的病例。生酮饮食通过减少ROS和RNS有效解决这些因素,增强抗氧化防御,改善线粒体功能,和调节炎症基因。此外,KD通过抑制NF-κB激活来抑制促炎细胞因子和趋化因子的产生,抑制NLRP3炎性体,增加大脑腺苷水平,mTOR通路抑制,上调PPAR的表达式,促进健康的肠道微生物群,同时强调健康脂肪的消费。KD可以被认为是癫痫患者的一种有希望的治疗干预措施,特别是在耐药癫痫病例中。由于其针对氧化应激和炎症机制的靶向方法。
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.