Document Detail


Niaspan increases axonal remodeling after stroke in type 1 diabetes rats.
MedLine Citation:
PMID:  22266016     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND OBJECTIVE: We investigated axonal plasticity in the bilateral motor cortices and the long term therapeutic effect of Niaspan on axonal remodeling after stroke in type-1 diabetic (T1DM) rats.
EXPERIMENTAL APPROACHES: T1DM was induced in young adult male Wistar rats via injection of streptozotocin. T1DM rats were subjected to 2h transient middle cerebral artery occlusion (MCAo) and were treated with 40 mg/kg Niaspan or saline starting 24 h after MCAo and daily for 28 days. Anterograde tracing using biotinylated dextran amine (BDA) injected into the contralateral motor cortex was performed to assess axonal sprouting in the ipsilateral motor cortex area. Functional outcome, SMI-31 (a pan-axonal microfilament marker), Bielschowsky silver and synaptophysin expression were measured. In vitro studies using primary cortical neuron (PCN) cultures and in vivo BDA injection into the brain to anterogradely label axons and terminals were employed.
RESULTS: Niaspan treatment of stroke in T1DM-MCAo rats significantly improved functional outcome after stroke and increased SMI-31, Bielschowsky silver and synaptophysin expression in the ischemic brain compared to saline treated T1DM-MCAo rats (p<0.05). Using BDA to anterograde label axons and terminals, Niaspan treatment significantly increased axonal density in ipsilateral motor cortex in T1DM-MCAo rats (p<0.05, n=7/group). Niacin treatment of PCN significantly increased Ang1 expression under high glucose condition. Niacin and Ang1 significantly increased neurite outgrowth, and anti-Ang1 antibody marginally attenuated Niacin induced neurite outgrowth (p=0.06, n=6/group) in cultured PCN under high glucose condition.
CONCLUSION: Niaspan treatment increased ischemic brain Ang1 expression and promoted axonal remodeling in the ischemic brain as well as improved functional outcome after stroke. Ang1 may partially contribute to Niaspan-induced axonal remodeling after stroke in T1DM-rats.
Authors:
Tao Yan; Michael Chopp; Xinchun Ye; Zhongwu Liu; Alex Zacharek; Yisheng Cui; Cynthia Roberts; Ben Buller; Jieli Chen
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Publication Detail:
Type:  Journal Article     Date:  2012-01-11
Journal Detail:
Title:  Neurobiology of disease     Volume:  46     ISSN:  1095-953X     ISO Abbreviation:  Neurobiol. Dis.     Publication Date:  2012 Apr 
Date Detail:
Created Date:  2012-03-12     Completed Date:  2012-11-20     Revised Date:  2014-09-22    
Medline Journal Info:
Nlm Unique ID:  9500169     Medline TA:  Neurobiol Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  157-64     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Axons / drug effects*,  physiology
Diabetes Mellitus, Type 1 / complications*,  physiopathology
Disease Models, Animal
Female
Infarction, Middle Cerebral Artery / complications,  drug therapy*,  pathology
Male
Neuronal Plasticity / drug effects*,  physiology
Niacin / analogs & derivatives,  pharmacology*
Pregnancy
Primary Cell Culture
Rats
Rats, Wistar
Vitamin B Complex / pharmacology
Grant Support
ID/Acronym/Agency:
P01 NS023393/NS/NINDS NIH HHS; P01 NS023393-22/NS/NINDS NIH HHS; R01 AG031811/AG/NIA NIH HHS; R01 AG031811-04/AG/NIA NIH HHS; R41 NS064708/NS/NINDS NIH HHS; R41 NS064708-01A2/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
12001-76-2/Vitamin B Complex; 59-67-6/Niacin
Comments/Corrections

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