Alteration of beta-amyloid and glutamate transporter in the brain of diabetes rats and the underlying mechanism / 中国医学科学院学报
Acta Academiae Medicinae Sinicae
; (6): 708-711, 2005.
Article
en Zh
| WPRIM
| ID: wpr-318831
Biblioteca responsable:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the alteration of beta-amyloid (Abeta) and glutamate transporter in the brain cortex of diabetes mellitus (DM) rats and the underlying mechanism.</p><p><b>METHODS</b>The rats were randomly divided into control, DM, DM +NaCl, and DM +LiCl groups and diabetes was induced by streptozotocin. The activity of glycogen synthase kinase-3 (GSK-3) and the function of glutamate transporter were measured by 32P-labelling. The amount of Abeta was determined by enzyme-linked immunosorbentassay.</p><p><b>RESULTS</b>In DM group, the level of Abeta40 increased (P < 0.01), but the function of glutamate transporter was impaired (P < 0.05). The activity of GSK-3 was stimulated (P < 0.05). Compared with DM group, the level of Abeta40 was restored (P < 0.01), and the function of glutamate transporter was enhanced (P < 0.05) in LiCl treated group, accompanied by a decreased activity of GSK-3.</p><p><b>CONCLUSION</b>Overproduction of Abeta and impaired glutamate transporter exist in DM rats, and increase of GSK-3 may play a crucial role in this process.</p>
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Índice:
WPRIM
Asunto principal:
Farmacología
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Distribución Aleatoria
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Corteza Cerebral
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Péptidos beta-Amiloides
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Ratas Sprague-Dawley
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Cloruro de Litio
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Sistema de Transporte de Aminoácidos X-AG
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Glucógeno Sintasa Quinasa 3
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Diabetes Mellitus Experimental
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Quimioterapia
Límite:
Animals
Idioma:
Zh
Revista:
Acta Academiae Medicinae Sinicae
Año:
2005
Tipo del documento:
Article