English  |  正體中文  |  简体中文  |  Items with full text/Total items : 16714/19009 (88%)
Visitors : 5633335      Online Users : 78
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31711


    標題: Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-kappa B/IL-6/synapsin I axis in traumatic brain injury rats
    作者: Chio, Chung-Ching
    Lin, Hung-Jung
    Tian, Yu-Feng
    Chen, Yu-Chieh
    Lin, Mao-Tsun
    Lin, Cheng-Hsien
    Chang, Ching-Ping
    Hsu, Chien-Chin
    貢獻者: Chi Mei Med Ctr, Dept Surg
    Chi Mei Med Ctr, Dept Emergency Med
    Southern Taiwan Univ Sci & Technol, Dept Biotechnol
    Chi Mei Med Ctr, Dept Surg, Div Gen Surg
    Chia Nan Univ Pharm & Sci, Dept Hlth & Nutr
    Chi Mei Med Ctr, Dept Med Res
    Meridigen Biotech Co Ltd
    Taipei Med Univ, PhD Program Neural Regenerat Med
    關鍵字: Brain injury
    Neuroprotection
    Neuroinflammation
    Exercise
    IL-6
    HSP70
    Synapsin I
    日期: 2017-04-24
    上傳時間: 2018-11-30 15:53:50 (UTC+8)
    出版者: Biomed Central Ltd
    摘要: Background: Despite previous evidence for a potent inflammatory response after a traumatic brain injury (TBI), it is unknown whether exercise preconditioning (EP) improves outcomes after a TBI by modulating inflammatory responses. Methods: We performed quantitative real-time PCR (qPCR) to quantify the genes encoding 84 cytokines and chemokines in the peripheral blood and used ELISA to determine both the cerebral and blood levels of interleukin-6 (IL-6). We also performed the chromatin immunoprecipitation (ChIP) assay to evaluate the extent of nuclear factor kappa-B (NF-kappa B) binding to the DNA elements in the IL-6 promoter regions. Also, we adopted the Western blotting assay to measure the cerebral levels of heat shock protein (HSP) 70, synapsin I, and beta-actin. Finally, we performed both histoimmunological and behavioral assessment to measure brain injury and neurological deficits, respectively. Results: We first demonstrated that TBI upregulated nine pro-inflammatory and/or neurodegenerative messenger RNAs (mRNAs) in the peripheral blood such as CXCL10, IL-18, IL-16, Cd-70, Mif, Ppbp, Ltd, Tnfrsf 11b, and Faslg. In addition to causing neurological injuries, TBI also upregulated the following 14 anti-inflammatory and/or neuroregenerative mRNAs in the peripheral blood such as Ccl19, Ccl3, Cxcl19, IL-10, IL-22, IL-6, Bmp6, Ccl22, IL-7, Bmp7, Ccl2, Ccl17, IL-1rn, and Gpi. Second, we observed that EP inhibited both neurological injuries and six proinflammatory and/or neurodegenerative genes (Cxcl10, IL-18, IL-16, Cd70, Mif, and Faslg) but potentiated four antiinflammatory and/or neuroregenerative genes (Bmp6, IL-10, IL-22, and IL-6). Prior depletion of cerebral HSP70 with gene silence significantly reversed the beneficial effects of EP in reducing neurological injuries and altered gene profiles after a TBI. A positive Pearson correlation exists between IL-6 and HSP70 in the peripheral blood or in the cerebral levels. In addition, gene silence of cerebral HSP70 significantly reduced the overexpression of NF-kappa B, IL-6, and synapsin I in the ipsilateral brain regions after an EP in rats. Conclusions: TBI causes neurological deficits associated with stimulating several pro-inflammatory gene profiles but inhibiting several anti-inflammatory gene profiles of cytokines and chemokines. Exercise protects against neurological injuries via stimulating an anti-inflammatory HSP70/NF-kappa B/IL-6/synapsin I axis in the injured brains.
    關聯: Journal of Neuroinflammation, v.14, pp.90
    Appears in Collections:[保健營養系(所) ] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML24View/Open
    s12974-017-0867-9.pdf4830KbAdobe PDF6View/Open


    All items in CNU IR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback