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    A translocator protein 18 kDa agonist protects against cerebral ischemia/reperfusion injury

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    s12974-017-0921-7.pdf
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    Author
    Li, Han-Dong
    Li, Minshu
    Shi, Elaine
    Jin, Wei-Na
    Wood, Kristofer
    Gonzales, Rayna
    Liu, Qiang
    Affiliation
    Univ Arizona, Coll Med, Dept Basic Med Sci
    Issue Date
    2017-07-28
    Keywords
    TSPO
    Etifoxine
    Neuroinflammation
    Cerebral ischemia
    
    Metadata
    Show full item record
    Publisher
    BIOMED CENTRAL LTD
    Citation
    A translocator protein 18 kDa agonist protects against cerebral ischemia/reperfusion injury 2017, 14 (1) Journal of Neuroinflammation
    Journal
    Journal of Neuroinflammation
    Rights
    © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    Background: Cerebral ischemia is a leading cause of death and disability with limited treatment options. Although inflammatory and immune responses participate in ischemic brain injury, the molecular regulators of neuroinflammation after ischemia remain to be defined. Translocator protein 18 kDa (TSPO) mainly localized to the mitochondrial outer membrane is predominantly expressed in glia within the central nervous system during inflammatory conditions. This study investigated the effect of a TSPO agonist, etifoxine, on neuroinflammation and brain injury after ischemia/reperfusion. Methods: We used a mouse model of middle cerebral artery occlusion (MCAO) to examine the therapeutic potential and mechanisms of neuroprotection by etifoxine. Results: TSPO was upregulated in Iba1(+) or CD11b(+) CD45(int) cells from mice subjected to MCAO and reperfusion. Etifoxine significantly attenuated neurodeficits and infarct volume after MCAO and reperfusion. The attenuation was pronounced in mice subjected to 30, 60, or 90 min MCAO. Etifoxine reduced production of pro-inflammatory factors in the ischemic brain. In addition, etifoxine treatment led to decreased expression of interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and inducible nitric oxide synthase by microglia. Notably, the benefit of etifoxine against brain infarction was ablated in mice depleted of microglia using a colony-stimulating factor 1 receptor inhibitor. Conclusions: These findings indicate that the TSPO agonist, etifoxine, reduces neuroinflammation and brain injury after ischemia/reperfusion. The therapeutic potential of targeting TSPO requires further investigations in ischemic stroke.
    ISSN
    1742-2094
    DOI
    10.1186/s12974-017-0921-7
    Version
    Final published version
    Sponsors
    American Heart Association [16SDG27250236]; National Science Foundation of China [81471535]; Ministry of Human Resources and Social Security of China [2016]; Tianjin Education Commission Foundation [14JCYBJC42000]; Tianjin Medical University Graduate Student Innovation Foundation [YJSCX201718]
    Additional Links
    http://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-017-0921-7
    ae974a485f413a2113503eed53cd6c53
    10.1186/s12974-017-0921-7
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