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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 |
| 顯示於類別: | [保健營養系(所) ] 期刊論文
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