2-chloro-n(6)-(3-iodobenzyl)adenosine-5--n-methyluronamide and Subarachnoid-Hemorrhage

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.

Topics: Adenosine; Adenosine A3 Receptor Agonists; Analysis of Variance; Animals; Brain Injuries; Enzyme-Linked Immunosorbent Assay; Fluorescent Antibody Technique; Male; Rats; Rats, Sprague-Dawley; Subarachnoid Hemorrhage