TY - JOUR
T1 - Adenosine A3 receptor agonist reduces early brain injury in subarachnoid haemorrhage
AU - Luo, Chunxia
AU - Yi, Bin
AU - Tao, Guocai
AU - Li, Mei
AU - Chen, Zhi
AU - Tang, Weihua
AU - Zhang, John H.
AU - Feng, Hua
N1 - Neuroreport. 2010 Sep 15;21(13):892-6. doi: 10.1097/WNR.0b013e32833dbd13. Research Support, Non-U.S. Gov't
PY - 2010/9/15
Y1 - 2010/9/15
N2 - 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.
AB - 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.
KW - adenosine A3 receptor agonist
KW - early brain injury
KW - inflammatory cytokines
KW - microglia
KW - subarachnoid haemorrhage
KW - Enzyme-Linked Immunosorbent Assay
KW - Rats
KW - Male
KW - Adenosine A3 Receptor Agonists/therapeutic use
KW - Rats, Sprague-Dawley
KW - Subarachnoid Hemorrhage/complications
KW - Adenosine/analogs & derivatives
KW - Animals
KW - Brain Injuries/drug therapy
KW - Analysis of Variance
KW - Fluorescent Antibody Technique
UR - http://www.scopus.com/inward/record.url?scp=77955912447&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77955912447&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/24080528-30ff-3706-8215-630ec7de28be/
U2 - 10.1097/WNR.0b013e32833dbd13
DO - 10.1097/WNR.0b013e32833dbd13
M3 - Article
C2 - 21150487
SN - 0959-4965
VL - 21
SP - 892
EP - 896
JO - NeuroReport
JF - NeuroReport
IS - 13
ER -