Sodium pyruvate ameliorates cognitive dysfunction by expanding hippocampal endogenous neural stem cells in tBCCAO mice.

After a stroke, many survivors experience post-stroke cognitive impairment (PSCI), a frequent clinical problem that might continue for an extended timeframe. Nerve regeneration is a crucial aspect of the body's self-repair mechanism following a stroke. While Sodium Pyruvate (SP) exhibits notable neuroprotective properties, its potential role in facilitating nerve regeneration requires further investigation. Thorough investigation into how cerebral ischemia-reperfusion injury is repaired and the function of SP in healing ischemic stroke damage. A temporary bilateral common carotid artery occlusion model (tBCCAO) was used to induce cerebral ischemic injury in mice. Laser scattering technique used to evaluate blood flow variations in the mouse brain. The water maze served as a tool to measure the learning and memory capabilities of the mice. The expansion of neural stem cells (NSCs) pool were evaluated through immunofluorescence, Western blot, and qPCR assays. SP significantly mitigates pathological brain tissue damage, enhances learning and memory in mice, stimulates NSC pool expansionin the hippocampal subgranular zone (SGZ) region, and upregulates the expression of SOX2, p300, H3K9ac, and DCX proteins in vivo. According to our findings, the mechanisms by which SP enhances the growth of internal NSCs and the maturation of immature neurons may involve the p300-H3K9ac-DCX signaling pathway, suggesting a new therapeutic target for stroke recovery.