Protective effect of polysaccharide peptide on cerebral ischemia-reperfusion injury in rats

In the present study, the protective effects and regulatory mechanism of polysaccharide peptide (PSP) were investigated in rats with cerebral ischemia-reperfusion (IR) injury. Neuroblastoma N2a cells were divided into five groups: Negative control; IR injury; PSP low dose treatment; PSP middle dose treatment; and PSP high dose treatment. In vitro, the cell viability was detected by an MTT assay. ELISA was performed to determine the activity of lactate dehydrogenase (LDH) and caspase-3. A cerebral IR injury model in vivo was established, and hematoxylin and eosin (H&E) staining, western blotting, neurological deficit score and cerebral infarction were assessed. The cell viability was markedly improved following treatment with PSP and the activity of LDH and caspase-3 was decreased following PSP administration (P<0.05). The in vivo studies determined that the neurological deficit score and cerebral infarction volume were reduced with the concentration of PSP increasing between 150 and 250 mg/kg. The H&E staining indicated that PSP was able to protect the nerve cells against the cerebral IR injury. In addition, PSP upregulated the decreased silent information regulator protein 1, peroxisome proliferator-activated receptor coactivator-1 and apoptosis regulator B-cell lymphoma 2 expression induced by cerebral IR injury. The protein expression level of caspase-3 and apoptosis regulator apoptosis regulator Bcl-2-like protein 4 was downregulated following PSP administration. These results suggested that PSP may improve nerve cell viability, enhance the neuroprotective role in cerebral IR injury and provide a novel approach for the treatment of cerebral IR injury.