USTHB, Faculty of Biological Sciences, Laboratory of Cellular and Molecular Biology, BP32, El Alia, Bab Ezzouar, 16111, Algiers, Algeria.
CRN2M UMR 7286, CNRS, Aix Marseille Université, 13344, Marseille Cedex 15, France.
Inflamm Res. 2016 Aug;65(8):623-34. doi: 10.1007/s00011-016-0945-y. Epub 2016 Apr 6.
Channelopathies due to the brain ion channel dysfunction is considered to be an important mechanism involved in various neurodegenerative diseases. In this study, we evaluated the ability of kaliotoxin (KTX) as K(+) channel blocker to induce neuro-inflammatory response and neurodegenerative alteration. We also investigate the effects of astaxanthin (ATX) against KTX disorders.
NMRI mice were injected with KTX (1 pg/kg, by i.c.v route) with or without pretreatment using ATX (80 mg/kg, o.p route).
Results showed that KTX was detected in cerebral cortex area due to its binding to the specific receptors (immunofluorescence analysis). It induced an activation of inflammatory cascade characterized by an increase of IL-6, TNFα, NO, MDA levels and NF-κB expression associated to a decrease of GSH level. The neuroinflammatory response is accompanied with cerebral alterations and blood-brain barrier (BBB) disruption. The use of ATX prior to the KTX exerts a preventive effect not only on the neuroinflammation but also on altered tissues and the BBB disruption.
Kaliotoxin is able to induce neurological disorders by blocking the K(+) ion channel, and ATX suppresses this alterations with down regulation of IL-6, TNF-α and NF-κB expression in the brain.
由于脑离子通道功能障碍导致的通道病被认为是多种神经退行性疾病的一个重要机制。在这项研究中，我们评估了卡利毒素（KTX）作为 K(+) 通道阻断剂诱导神经炎症反应和神经退行性改变的能力。我们还研究了虾青素（ATX）对 KTX 紊乱的作用。
NMRI 小鼠通过脑室内途径（i.c.v）注射 KTX（1 pg/kg），或预先使用 ATX（80 mg/kg，口服）预处理。
结果表明，KTX 由于与特定受体结合而在大脑皮层区域被检测到（免疫荧光分析）。它诱导了炎症级联的激活，表现为 IL-6、TNFα、NO、MDA 水平和 NF-κB 表达的增加，同时 GSH 水平降低。神经炎症反应伴随着大脑的改变和血脑屏障（BBB）的破坏。在 KTX 之前使用 ATX 不仅对神经炎症，而且对改变的组织和 BBB 的破坏都具有预防作用。
卡利毒素通过阻断 K(+) 离子通道引起神经紊乱，而 ATX 通过下调脑内 IL-6、TNF-α 和 NF-κB 的表达来抑制这些改变。
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