Little is known about K⁺ regulation playing major roles in the propagation of nerve impulses, as well as in apoptosis and inflammasome activation involved in neurodegeneration. As increased levels of 7-ketocholesterol (7KC), 24S-hydroxycholesterol (24S-OHC) and tetracosanoic acid (C24:0) have been observed in patients with neurodegenerative diseases, we studied the effect of 24 and/or 48 h of treatment with 7KC, 24S-OHC and C24:0 on Kv3.1b potassium channel level, intracellular K⁺ concentration, oxidative stress, mitochondrial dysfunction, and plasma membrane permeability in 158N oligodendrocytes and BV-2 microglial cells. In 158N cells, whereas increased level of Kv3.1b was only observed with 7KC and 24S-OHC but not with C24:0 at 24 h, an intracellular accumulation of K⁺ was always detected. In BV-2 cells treated with 7KC, 24S-OHC and C24:0, Kv3.1b level was only increased at 48 h; intracellular K⁺ accumulation was found at 24 h with 7KC, 24S-OHC and C24:0, and only with C24:0 at 48 h. Positive correlations between Kv3.1b level and intracellular K⁺ concentration were observed in 158N cells in the presence of 7KC and 24S-OHC, and in 7KC-treated BV-2 cells at 48 h. Positive correlations were also found between Kv3.1b or the intracellular K⁺ concentration, overproduction of reactive oxygen species, loss of transmembrane mitochondrial potential and increased plasma membrane permeability in 158N and BV-2 cells. Our data support that the lipid environment affects Kv3.1b channel expression and/or functionality, and that the subsequent rupture of K⁺ homeostasis is relied with oligodendrocytes and microglial cells damages.

关于K ⁺调节在神经冲动的传播，以及神经变性涉及的凋亡和炎症小体活化中起主要作用的了解甚少。由于在神经退行性疾病患者中观察到7-酮胆固醇（7KC），24S-羟基胆固醇（24S-OHC）和四癸酸（C24：0）的水平升高，因此我们研究了24和/或48 h的神经退行性疾病治疗的效果在158N少突胶质细胞和BV-2小胶质细胞中，Kv3.1b钾通道水平，细胞内K ⁺浓度，氧化应激，线粒体功能障碍和质膜通透性分别为7KC，24S-OHC和C24：0 。在158N细胞，而增加Kv3.1b的水平仅与7KC和24S-OHC但不与C24观察到：0在第24小时，K的细胞内积聚⁺始终被检测到。在用7KC，24S-OHC和C24：0处理的BV-2细胞中，Kv3.1b水平仅在48 h时升高；7KC，24S-OHC和C24：0在24 h时发现细胞内K ⁺积累，而在48 h仅在C24：0时发现。在存在7KC和24S-OHC的情况下，在158N细胞中以及在48 h处理7KC的BV-2细胞中，观察到Kv3.1b水平与细胞内K ⁺浓度之间呈正相关。在Kv3.1b或细胞内K ⁺之间也发现正相关158N和BV-2细胞的浓度，活性氧的过量生产，跨膜线粒体电位的丧失和质膜通透性的增加。我们的数据支持脂质环境影响Kv3.1b通道的表达和/或功能，并且随后的K ⁺稳态破裂取决于少突胶质细胞和小胶质细胞的损害。