title: 3-n-Butylphthalide (NBP) attenuated neuronal autophagy and amyloid-β expression in diabetic mice subjected to brain ischemia.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Neurology, Shanghai Jiaotong University Affillilated Sixth People's Hospital, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Zhang
authors.forename: Weihong
authors.initials: W
authors.lastname: Yan
authors.forename: Qiang
authors.initials: Q
authors.lastname: Li
authors.forename: Jianliang
authors.initials: J
authors.lastname: Fu
authors.forename: Kangyong
authors.initials: K
authors.lastname: Liu
authors.forename: Weiping
authors.initials: W
authors.lastname: Jia
authors.forename: Xiaojiang
authors.initials: X
authors.lastname: Sun
authors.forename: Xueyuan
authors.initials: X
authors.lastname: Liu
mesh_terms: D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors* / Q000378:metabolism; D000818:Animals; D001343:Autophagy / Q000187:drug effects* / Q000502:physiology; D001572:Benzofurans / Q000008:administration & dosage* / Q000627:therapeutic use; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D003704:Dementia / Q000150:complications / Q000378:metabolism / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism* / Q000473:pathology*; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009410:Nerve Degeneration / Q000150:complications / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D011897:Random Allocation; D016896:Treatment Outcome
chemical_list: D016229:Amyloid beta-Peptides; D001572:Benzofurans; D018696:Neuroprotective Agents; C027125:3-n-butylphthalide