Effect of prothymosin α on neuroplasticity following cerebral ischemia‑reperfusion injury

Prothymosin α (ProT), a highly acidic nuclear protein with multiple cellular functions, has shown potential neuroprotective properties attributed to its anti‑necrotic and anti‑apoptotic activities. The present study aimed to investigate the beneficial effect of ProT on neuroplasticity after ischemia‑reperfusion injury and elucidate its underlying mechanism of action. Primary cortical neurons were either treated with ProT or overexpressing ProT by gene transfection and exposed to oxygen‑glucose deprivation for 2 h in vitro. Immunofluorescence staining for ProT and MAP‑2 was performed to quantify ProT protein expression and assess neuronal arborization. Mice treated with vehicle or ProT (100 µg/kg) and ProT overexpression in transgenic mice received middle cerebral artery occlusion for 50 min to evaluate the effect of ProT on neuroplasticity‑associated protein following ischemia‑reperfusion injury. The results demonstrated that in cultured neurons ProT significantly increased neurite lengths and the number of branches, accompanied by an upregulation mRNA level of brain‑derived neurotrophic factor. Furthermore, ProT administration improved the protein expressions of synaptosomal‑associated protein, 25 kDa and postsynaptic density protein 95 after ischemic‑reperfusion injury in vivo. These findings suggested that ProT can potentially induce neuroplasticity effects following ischemia‑reperfusion injury.