有哪些信誉好的足球投注网站a β-lactam antibiotic dampens excitotoxic inflammatory cns damage in a mouse model of multiple sclerosisβ-lactam抗生素抑制了excitotoxic炎性中枢神经系统损伤的小鼠模型多发性硬化症.pdfVIP
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a β-lactam antibiotic dampens excitotoxic inflammatory cns damage in a mouse model of multiple sclerosisβ-lactam抗生素抑制了excitotoxic炎性中枢神经系统损伤的小鼠模型多发性硬化症
A b-Lactam Antibiotic Dampens Excitotoxic Inflammatory
CNS Damage in a Mouse Model of Multiple Sclerosis
1. 1. 2,4 1 1
Nico Melzer *, Sven G. Meuth , Delany Torres-Salazar , Stefan Bittner , Alla L. Zozulya , Christian
1 3 3 2 1
Weidenfeller , Alexandra Kotsiari , Martin Stangel , Christoph Fahlke , Heinz Wiendl *
¨ ¨
1 Department of Neurology, University of Wurzburg, Wurzburg, Germany, 2 Department of Neurophysiology, Medizinische Hochschule Hannover, Hannover, Germany,
3 Department of Neurology, Medizinische Hochschule Hannover, Hannover, Germany, 4 Department of Neurobiology, University of Pittsburgh School of Medicine,
Pittsburgh, Pennsylvania, United States of America
Abstract
In multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE), impairment of glial
‘‘Excitatory Amino Acid Transporters’’ (EAATs) together with an excess glutamate-release by invading immune cells causes
excitotoxic damage of the central nervous system (CNS). In order to identify pathways to dampen excitotoxic inflammatory
CNS damage, we assessed the effects of a b-lactam antibiotic, ceftriaxone, reported to enhance expression of glial EAAT2, in
‘‘Myelin Oligodendrocyte Glycoprotein’’ (MOG)-induced EAE. Ceftriaxone profoundly ameliorated the clinical course of
murine MOG-induced EAE both under preventive and therapeutic regimens. However, ceftriaxone had impact neither on
EAAT2 protein expression levels in several brain areas, nor on the radioactive glutamate uptake capacity in a mixed primary
glial cel
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