Protective effect of bradykynin postconditioning on neurons in rats following cardiopulmonary resuscitation

Abstract

Objective To evaluate the protective effect of delayed bradykinin post-conditioning on hippocampus CA1 neurons of rat following cardiopulmonary resuscitation. Methods A total of 24 male SD rats were randomly (random number) divided into sham group, restoration of spontaneous circulation group (ROSC) and bradykinin post-conditioning group (BR-P) , using random number method. Cardiac arrest was induced by suffocation method with vecuronium bromide injection to paralyze the respiratory movement. Cardiopulmonary resuscitation was performed 6 min after cardiac arrest. Two days after ROSC, bradykinin (150 μg/kg) was administrated intraperitoneally in BR-P group and the equivalent volume of saline was injected instead in ROSC group. Three days after ROSC, neurological function of rats was evaluated with neurological deficit score (NDS). And then brain tissue was taken for DAPI/Bax, Bcl-2 and Caspase-3 with double immunofluorescence staining and neuron apoptosis and Bax, Bcl-2 and Caspase-3 expression in CA1 region of hippocampus were assessed. The results were expressed as (±s) and one way analysis of variance was employed for comparison among groups. Results Compared with sham group, ROSC group exhibited a lower NDS score (60.13 vs. 80.00, P <0.01) , higher Bax and Caspase-3 expression in CA1 region (56.70 vs. 37.39, P <0.01; 43.46 vs. 37.29, P <0.01) and lower expression of Bcl-2 (41.90 vs. 47.52, P <0.01). Compared to ROSC group, there were higher NDS score (69.75 vs. 60.13, P < 0.01) , lower Bax and Caspase-3 expression (51.34 vs. 56.70, P <0.05; 38.90 vs. 43.46, P <0.05) and enhanced Bcl-2 expression (41.90 vs. 47.52, P <0.05) in BR-P group. Conclusions Bradykinin post-conditioning can exert neuroprotective effects on rats after CPR and the neuroprotection is likely associated with down-regulation of Bax and Caspase-3, and activation of Bacl-2, inhibiting neuron apoptosis in CA1 region. Key words: Bradykinin; Postconditioning; Cardiac arrest; Cardiopulmonary resuscitation; Neuroprotective effect