Journal
NEUROCHEMICAL RESEARCH
Volume 46, Issue 4, Pages 888-904Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-021-03233-0
Keywords
Ischemic stroke; S-oxiracetam; Apoptosis; alpha 7nAChR; Learning and memory
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Funding
- National Natural Science Foundation of China [81701313]
- Fundamental Research Funds for the Central Universities [2242020K40175]
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This study confirmed the protective effect of S-ORC on cognitive recovery after MCAO/R in rats, and identified alpha 7nAChR and PI3K as key molecules mediating the cognitive restoration induced by S-ORC.
S-oxiracetam (S-ORC), a nootropic drug, was used to protect against ischemic stroke by lessening the blood brain barrier dysfunction and inhibiting neuronal apoptosis. However, the potential effects of S-ORC in the recovery of cognitive functions after ischemic stroke and the underlying mechanisms remains unclear. In this study, middle cerebral artery occlusion/reperfusion (MCAO/R) in rats was used as the animal model. By using Y-maze test, Morris water maze, triphenyl tetrazolium chloride (TTC) staining, terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate (dUTp) nick end labeling (TUNEL) assay, hematoxylin and eosin, immunohistochemical staining and western blot to evaluate the protective effect of S-ORC on cognitive recovery, we were able to confirm that S-ORC ameliorated spatial learning impairment, tissue loss, and hippocampal neuronal apoptosis and injury induced by MCAO/R in rats. These cognitive effects were achieved by restoring the normal function of synaptophysin and increasing PSD95 expression in the hippocampus. Furthermore, we found that methyllycaconitine, the antagonist of alpha 7 nicotinic acetylcholine receptor (alpha 7nAChR), and LY294002, the inhibitor of phosphoinositide 3-kinase (PI3K), were able to block the cognitive effects of S-ORC after MCAO/R in rats. In conclusion, alpha 7nAChR and PI3K are key molecules that mediated the signaling pathway leading to S-ORC-induced cognitive restoration after MCAO/R.
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