3-n-Butylphthalide (NBP) attenuated neuronal autophagy and amyloid-β expression in diabetic mice subjected to brain ischemia.

Autor:	Zhang T; Department of Neurology, Shanghai Jiaotong University Affillilated Sixth People's Hospital, China., Yan W, Li Q, Fu J, Liu K, Jia W, Sun X, Liu X
Jazyk:	angličtina
Zdroj:	Neurological research [Neurol Res] 2011 May; Vol. 33 (4), pp. 396-404.
DOI:	10.1179/1743132810Y.0000000006
Abstrakt:	Objective: The aim of this study was to investigate the protective effect of dl-3-n-butylphthalide (NBP) on brain damage in streptozotocin (STZ)-induced diabetic mice subjected to cerebral ischemia. Methods: we pretreated diabetic mice with NBP orally for 4 weeks prior and 2 days after transient common carotid artery occlusion (CCAO) operation. Immunohistochemistry and transmission electron microscopy were performed to investigate the neuronal loss, astrocytes activation, amyloid-beta (Abeta) protein expression, and autophagy activation. Results: The results showed that diabetes increased stroke-induced neuronal loss, astrocytes activation, Abeta generation, and autophagy activity, while NBP administration attenuated these changes. Immunofluorescence double staining of Abeta with autophagosome-specific antibody LC3 showed that most elevated Abeta(+) signal was co-localized with LC3(+) signal. Conclusion: Our finding suggests that NBP attenuates Abeta generation promoted by diabetes in ischemia might act through inhibiting abnormally activated neuronal autophagy. Therefore, treatment with NBP to modulate autophagy might provide a novel therapeutic strategy for diabetes by preventing ischemic brain damage and depressing the risk of post-stroke dementia.
Databáze:	MEDLINE
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