Oleuropein Mitigates Radiation-Induced Neurodegeneration in Rats by Modulating Oxidative, Vascular, and Apoptotic...

Radiation (RAD) is widely used in medicine but poses risks to non-regenerative tissues such as the brain. This study aimed to investigate the neuroprotective effects of oleuropein (OLE) against RAD-induced brain injury in rats by evaluating oxidative stress, apoptosis, and vascular responses. Thirty-two male Wistar rats were randomly assigned to four groups: Control, RAD (6 Gy cranial irradiation), RAD+OLE (50 mg/kg/day oral gavage, initiated 1 week before and continued 3 weeks after irradiation), and OLE alone. Histopathological (H&E, PAS), immunohistochemical (Cyclin-D1, CD31, GLUT-1), biochemical (serum CK-BB), and molecular (Bax, Bcl-2 mRNA via RT-qPCR) analyses were performed. RAD exposure resulted in significant neuronal degeneration, upregulation of Cyclin-D1, CD31, and GLUT-1 expression, increased pro-apoptotic Bax, decreased anti-apoptotic Bcl-2, and elevated serum CK-BB (p < 0.05). OLE treatment significantly attenuated these alterations, restoring brain tissue architecture, normalizing PAS staining, downregulating apoptotic and vascular markers, and reducing CK-BB levels (p < 0.05). These findings suggest that OLE exerts potent neuroprotective effects against RAD-induced brain damage by attenuating oxidative stress, vascular activation, and apoptosis. OLE may serve as a promising adjuvant in radiotherapy to reduce central nervous system (CNS) side effects. Further studies focusing on functional outcomes and dose optimization are warranted.