Arbutin Improves Functional Recovery and Attenuates Glial Activation in Lysolecethin-Induced Demyelination Model in Rat Optic Chiasm

Neuroinflammation, glial activation, and oxidative injury are the main pathological mechanisms of demyelination in multiple sclerosis (MS). Arbutin, a natural polyphenol compound, possesses antioxidant, anti-inflammatory, and neuroprotective properties whose therapeutic potential has not been studie...

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Veröffentlicht in:	Molecular neurobiology 2020-07, Vol.57 (7), p.3228-3242
Hauptverfasser:	Ebrahim-Tabar, Forough, Nazari, Atena, Pouramir, Mahdi, Ashrafpour, Manuchehr, Pourabdolhossein, Fereshteh
Format:	Artikel
Sprache:	eng
Schlagworte:	Animal models Animals Antioxidants Arbutin - pharmacology Arbutin - therapeutic use Astrocytes - drug effects Astrocytes - metabolism Biomedical and Life Sciences Biomedicine Cell Biology Cytokines - metabolism Demyelinating Diseases - chemically induced Demyelinating Diseases - drug therapy Demyelinating Diseases - metabolism Demyelination Disease Models, Animal Evoked Potentials, Visual - drug effects GA-binding protein Gene expression Glial fibrillary acidic protein IL-1β Inflammation Injection Interleukin 1 Interleukin 10 Interleukin 17 Latency Life Sciences & Biomedicine Lysophosphatidylcholines Male Microglia - drug effects Microglia - metabolism Multiple sclerosis Myelin Neurobiology Neurology Neuronal-glial interactions Neuroprotection Neurosciences Neurosciences & Neurology Nitric-oxide synthase Olig2 protein Optic chiasm Optic Chiasm - drug effects Optic Chiasm - metabolism Oxidative stress Rats Rats, Wistar Recovery of function Recovery of Function - drug effects Science & Technology Tumor necrosis factor-α Visual evoked potentials
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