Adenosine A3 receptor agonist reduces early brain injury in subarachnoid haemorrhage

Chunxia Luo, Bin Yi, Guocai Tao, Mei Li, Zhi Chen, Weihua Tang, John H. Zhang, Hua Feng

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Inflammation plays an important role in the pathogenesis of early brain injury after subarachnoid haemorrhage. Adenosine A3 receptor (A3R) activation produces anti-inflammatory effects. In this study, the effects of a selective A3R agonist, 2-chloro-N6-(3-iodobenzyl)-adenosine-5′-N- methyluronamide (CL-IB-MECA), on early brain injury and inflammatory response after subarachnoid haemorrhage were studied. Our results showed that mortality, neurological impairment and brain oedema were significantly attenuated after the administration of CL-IB-MECA. Moreover, treatment with CL-IB-MECA inhibited microglial activation and reduced the expression of proinflammatory cytokines including tumour necrosis factor-α and interleukin-1β. These data suggest that activation of A3R provides a neuroprotective effect against brain injury after subarachnoid haemorrhage, and that these effects may be associated with the anti-inflammatory properties of A3R. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
    Original languageEnglish
    Pages (from-to)892-896
    Number of pages5
    JournalNeuroReport
    Volume21
    Issue number13
    DOIs
    StatePublished - Sep 15 2010

    ASJC Scopus Subject Areas

    • General Neuroscience

    Keywords

    • adenosine A3 receptor agonist
    • early brain injury
    • inflammatory cytokines
    • microglia
    • subarachnoid haemorrhage
    • Enzyme-Linked Immunosorbent Assay
    • Rats
    • Male
    • Adenosine A3 Receptor Agonists/therapeutic use
    • Rats, Sprague-Dawley
    • Subarachnoid Hemorrhage/complications
    • Adenosine/analogs & derivatives
    • Animals
    • Brain Injuries/drug therapy
    • Analysis of Variance
    • Fluorescent Antibody Technique

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