Lithium ameliorates rat spinal cord injury by suppressing glycogen synthase kinase-3β and activating heme oxygenase-1 / 대한해부학회지
Anatomy & Cell Biology
; : 207-213, 2017.
Article
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| WPRIM
| ID: wpr-50231
Biblioteca responsable:
WPRO
ABSTRACT
Glycogen synthase kinase (GSK)-3β and related enzymes are associated with various forms of neuroinflammation, including spinal cord injury (SCI). Our aim was to evaluate whether lithium, a non-selective inhibitor of GSK-3β, ameliorated SCI progression, and also to analyze whether lithium affected the expression levels of two representative GSK-3β–associated molecules, nuclear factor erythroid 2-related factor-2 (Nrf-2) and heme oxygenase-1 (HO-1) (a target gene of Nrf-2). Intraperitoneal lithium chloride (80 mg/kg/day for 3 days) significantly improved locomotor function at 8 days post-injury (DPI); this was maintained until 14 DPI (P<0.05). Western blotting showed significantly increased phosphorylation of GSK-3β (Ser9), Nrf-2, and the Nrf-2 target HO-1 in the spinal cords of lithium-treated animals. Fewer neuropathological changes (e.g., hemorrhage, inflammatory cell infiltration, and tissue loss) were observed in the spinal cords of the lithium-treated group compared with the vehicle-treated group. Microglial activation (evaluated by measuring the immunoreactivity of ionized calcium-binding protein-1) was also significantly reduced in the lithium-treated group. These findings suggest that GSK-3β becomes activated after SCI, and that a non-specific enzyme inhibitor, lithium, ameliorates rat SCI by increasing phosphorylation of GSK-3β and the associated molecules Nrf-2 and HO-1.
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Texto completo:
1
Base de datos:
WPRIM
Asunto principal:
Fosforilación
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Médula Espinal
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Traumatismos de la Médula Espinal
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Western Blotting
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Glucógeno Sintasa
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Cloruro de Litio
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Glucógeno Sintasa Quinasas
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Hemo-Oxigenasa 1
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Glucógeno
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Hemo
Límite:
Animals
Idioma:
En
Revista:
Anatomy & Cell Biology
Año:
2017
Tipo del documento:
Article