Anti‑Nogo‑A antibody promotes brain function recovery after cardiopulmonary resuscitation in rats by reducing apoptosis.

Brain injury after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) is the main cause of neurological dysfunction and death in cardiac arrest. To assess the effect of Nogo‑A antibody on brain function in rats following CPR and to explore the underlying mechanisms, CA/CPR (ventricular fibrillation) rats were divided into the CPR+Nogo‑A, CPR+saline and sham groups. Hippocampal caspase‑3 levels were detected by RT‑PCR and immunoblotting. Next, Nogo‑A, glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cysteinyl aspartate specific proteinase‑12 (casapse‑12), Bcl‑2 and Bax protein levels in the hippocampus were detected by immunoblotting. Coronal brain sections were analyzed by TUNEL assay to detect apoptosis at 72 h, while Nissl staining and electron microscopy were performed to detect Nissl bodies and microstructure at 24 h, respectively. Finally, rats were assessed for neurologic deficits at various times. Nissl staining revealed morphological improvement after Nogo‑A antibody treatment. Sub‑organelle structure was preserved as assessed by electron microscopy in model animals post‑antibody treatment; neurological function was improved as well (P<0.05), while the apoptosis index was decreased (26.2±9.85 vs. 46.6±12.95%; P<0.05). Hippocampal caspase‑3 mRNA and protein, Nogo‑A protein levels were significantly decreased after antibody treatment (P<0.05). Hippocampal Nogo‑A expression was positively correlated with caspase‑3 (Pearson's correlation; r=0.790, P=0.000). Hippocampal GRP78 and Bcl‑2 protein levels were higher after antibody treatment than these levels noted in the model animals (P<0.05), while CHOP, caspase‑12 and Bax levels were reduced (P<0.05). Nogo‑A antibody ameliorates neurological function after restoration of spontaneous circulation (ROSC), possibly by suppressing apoptosis induced by endoplasmic reticulum stress.