Abstract
We evaluated the effects of a non-specific potassium channel blocker, 4-aminopyridine (4-AP), on chronic experimental autoimmune encephalomyelitis (chEAE) and relapsing remitting EAE (rrEAE) in mice. 4-AP did not affect chEAE, but ameliorated rrEAE, particularly in the relapsing phase. Disease amelioration was confirmed pathologically, and glial fibrillary acidic protein expression was observed to be downregulated in 4-AP-treated mice. In the recall response, a T-cell proliferative response was not inhibited; however, Th1/Th17 polarization was attenuated. 4-AP is currently accepted as an anti-symptomatic drug only in the chronic phase of multiple sclerosis (MS); however, its use in the active phase of MS should be considered.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
