Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-kappa B/IL-6/synapsin I axis in traumatic brain injury rats

doi:10.1186/s12974-017-0867-9

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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
显示于类别:	[保健營養系(所) ] 期刊論文

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