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Introduction: Focal cerebral cortical infarction causes β-amyloid (Aβ) deposition and secondary neuronal degeneration in the ipsilateral thalamus. The present study aimed to investigate the protective effects of liraglutide, a long-acting glucagon-like peptide-1 (GLP-1) analogue, on Aβ deposits and secondary neuron damage in thalamus after cerebral infarction.Methods: Sixteen male Sprague-Dawley rats were subjected to distal middle cerebral artery occlusion (MCAO) and then randomly divided into liraglutide and vehicle groups and 8 sham-operated rats as control. At 1 hour after MCAO, rats were subcutaneously injected with liraglutide (100 μg/kg/d) and isopyknic vehicle, respectively, then continuously injected once a day for 7 days. Sensory function and secondary thalamic damage were assessed with adhesive-removal test, Nissl staining and immunostaining. Terminal-deoxynucleotidyl transferase-mediated nick end labelling (TUNEL) staining and Western blot were employed to detect the neuronal apoptosis at 7 days after MCAO.Results: At 7 days after MCAO, liraglutide decreased the mean time of adhesive-removal at left forepaw compared with the vehicle group (P < 0.05). Treatment with liraglutide reduced Aβ deposition compared with that in the vehicle group (P < 0.05). The number of intact neurons in the ipsilateral thalamus was decreased compared with the control group at 7 days post-MCAO, liraglutide significantly improved the number of intact neurons compared with the vehicle group (P < 0.05). Liraglutide decreased the glial fibrillary acidic protein (GFAP)-positive area and the number of ionized calcium bindingadaptor molecule-1 (Iba-1)-positive cells in the ipsilateral thalamus compared with the vehicle group (P < 0.05). Liraglutide significantly decreased the number of TUNEL-positive neurons in the ipsilateral thalamus compared with the vehicle group (P < 0.05). Consistent with the TUNEL staining results, liraglutide increased the ratio of Bcl-2/Bax (P < 0.05) and decreased the expression level of cleaved Caspase-3 relative to the vehicle group (P < 0.05).Conclusions: Liraglutide reduces Aβ deposits in the ipsilateral thalamus, improvesthe secondary thalamic damage and neurological deficit after cerebral infarction.