Exogenous adenosine facilitates neuroprotection and functional recovery following cerebral ischemia in rats

Cerebral ischemia causes physiological and biochemical cellular changes that ultimately result in structural and functional damage to hippocampal neurons. Ischemia also raises endogenous adenosine release that in turn has neuroprotective effects. The purpose of this study was to evaluate the effect of exogenous adenosine on mitigating neuronal lesions to the CA1 region of hippocampus and A2A protein expression following cerebral I/R in rats.

Male Wistar rats were randomly assigned to three experimental groups (sham, ischemia + control, and ischemia + adenosine). A daily dose of adenosine (0.1 mg/ml/kg, i.p.) was administered starting 24 h post-ischemia for 7 days. Ischemia was induced by occlusion of both common carotid arteries for 45 min. Cresyl violet and Hematoxylin Eosin staining were used to assess lesion extent and location. To investigate the expression and protein levels, immunohistochemistry and enzyme-linked immunosorbent assay method was used.

The cerebral ischemia caused neuronal loss in the CA1 region and reduced sensorimotor functions in lesion animals. Injection of adenosine significantly diminished cell death and improved sensorimotor functional recovery. Moreover, the expression and concentration of A2A protein was significantly greater in the adenosine group compared to the ischemia group.

This study showed that the administration of exogenous adenosine promotes protection against cell death and supports functional recovery following ischemic injury.