Effect of prothymosin on neuroplasticity following cerebral ischemia-reperfusion injury

Prothymosin alpha (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 mu g/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.