Abstract:Objective: To investigate the role of A1 adenosine receptor (A1AR) in secondary brain injury (SBI) induced by intracranial hemorrhage (ICH). Methods: Thirty adult male SD rats were randomized into sham operation group, ICH group, agonist group [A1 adenosine receptor agonist N (6) -cyclohexylflavin, R-PIA] and antagonist group (A1 adenosine receptor antagonist 8-phenyl-1, 3-dipropylxanthine, 8-PT), with 6 rats in each group. A collagenase-induced ICH model was established. The agonists and antagonists were administered 30 minutes before modeling and examinations were performed 48 hours later. The expressions of A1AR, active Caspase-3, albumin, B cell lymphoma 2 (Bcl-2) and Bax were detected by Western blot. The apoptosis of neurons was observed by TdT-mediated dUTP nick-end labeling (TUNEL). The degree of brain edema was evaluated by wet/dry ratio. Results: The expression of A1AR in agonist group was significantly up-regulated (P=0.000), while that in antagonist group was down-regulated. In agonist group, apoptosis decreased (P=0.003), and the levels of active Caspase-3 and albumin decreased (t=4.649, P=0.043; t=24.89, P=0.001). In the antagonist group, apoptosis increased, and the levels of active Caspase-3 and albumin were up-regulated (t=12.49, P=0.006; t=8.501, P=0.013). In agonist group, Bcl-2 expression increased (t=14.13, P=0.005), Bax expression decreased, and the degree of brain edema decreased (P=0.007). Conclusion: Activation of A1AR can increase the expression of Bcl-2, relieve brain edema, reduce nerve cell apoptosis and inhibit secondary brain injury.
