We have located links that may give you full text access.
K(+) channel blocker-induced neuroinflammatory response and neurological disorders: immunomodulatory effects of astaxanthin.
Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.] 2016 August
OBJECTIVE: 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.
MATERIAL AND TREATMENT: 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: 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.
CONCLUSIONS: 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.
MATERIAL AND TREATMENT: 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: 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.
CONCLUSIONS: 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.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app