上海大学陈雨研究团队报道了纳米工程，超小和催化六氰铁酸钾钙神经保护和颞叶癫痫治疗。该项研究成果发表在2025年2月25日出版的《科学通报》上。

在此，研究团队设计并制造了超小的六氰高铁酸钾钙（III）纳米颗粒，命名为KCaHNPs，其具有广谱的酶活性，类似于超氧化物歧化酶、过氧化氢酶、过氧化物酶和谷胱甘肽过氧化物酶。KCaHNPs有效地中和过多的活性氧，减轻线粒体功能障碍，维持神经元完整性，防止细胞凋亡。重要的是，KCaHNPs显著降低了tle大鼠的神经元损伤、凋亡、铁凋亡和胶质细胞活化，从而改善了空间和短期记忆，并减少了癫痫的高兴奋性。预防性部署KCaHNPs可显著降低癫痫发作的频率和持续时间，延长初始癫痫发作前的潜伏期，增强海马CA3区的神经功能。总的来说，这些发现强调了KCaHNPs通过增强抗氧化应激和炎症的细胞防御机制来减轻TLE的有效治疗和预防作用。这种创新的方法有望成为一种全面有效的治疗颞叶癫痫和其他潜在的复杂神经系统疾病的策略。

据悉，海马硬化是颞叶癫痫（TLE）发病机制的关键组成部分，其特征是海马神经元丢失、氧化应激、神经胶质细胞增殖和炎症反应。传统的治疗策略，主要涉及抗癫痫药物，面临着包括无效、药物耐受性和不良反应，使病情管理复杂化等挑战。

附：英文原文

Title: Nanoengineered, ultrasmall and catalytic potassium calcium hexacyanoferrate for neuroprotection and temporal lobe epilepsy treatment

Author: Fuxue Chen a, Wei Feng a b, Yu Chen a b d

Issue&Volume: 2025/02/25

Abstract: Hippocampal sclerosis, characterized by significant hippocampal neuronal loss, oxidative stress, glial cell proliferation, and inflammatory responses, constitutes a pivotal component in the pathogenesis of temporal lobe epilepsy (TLE). Traditional treatment strategies, mainly involving anti-epileptic drugs, face challenges including ineffectiveness, drug tolerance, and adverse reactions, complicating management of the condition. Herein, we design and engineer ultrasmall potassium calcium hexacyanoferrate (III) nanoparticles, designated as KCaHNPs, which feature a broad spectrum of enzymatic activities analogous to superoxide dismutase, catalase, peroxidase, and glutathione peroxidase. KCaHNPs efficiently neutralize excessive reactive oxygen species, mitigate mitochondrial dysfunction, maintain neuronal integrity, and prevent apoptosis. Importantly, KCaHNPs significantly reduce neuronal damage, apoptosis, ferroptosis, and glial cells activation in TLE-afflicted rats, thereby improving spatial and short-term memory, and diminishing epileptic hyperexcitability. Prophylactic deployment of KCaHNPs markedly decreases the frequency and duration of seizures, extends the latency period before the onset of initial seizures, and enhances neural functions within the hippocampal CA3 area. Collectively, these findings underscore the potent therapeutic and prophylactic efficacy of KCaHNPs in mitigating TLE by bolstering cellular defense mechanisms against oxidative stress and inflammation. This innovative approach holds promise as a comprehensive and efficacious strategy for managing temporal lobe epilepsy and potentially other complex neurological disorders.

DOI: 10.1016/j.scib.2025.02.036

Source: https://www.sciencedirect.com/science/article/abs/pii/S2095927325002026