Fırat AŞIR, Zeynep TÜRE, Gül Ebru AYDENİZ ACAR, Hayat AYAZ, Ayşenur SEVİNÇ AKDENİZ, Mehmet ÖLMEZ, Esma YILDIRIM, Mehmet ZÜLFİ DEMİR
Kocaeli Üniversitesi Sağlık Bilimleri Dergisi - 2026;12(1):56-61
Objective: Traumatic brain injury (TBI) remains a major cause of mortality and disability worldwide, with secondary injury mechanisms contributing significantly to neurodegeneration. The hippocampus is particularly vulnerable to these delayed processes, including oxidative stress, neuroinflammation, and astroglial activation. Nebivolol, a third-generation beta?-adrenergic antagonist with nitric oxide -mediated vasodilatory properties, has been proposed to exhibit therapeutic potential in neural injury models. This study aimed to evaluate the therapeutic effects of nebivolol on hippocampal injury following experimental TBI, with a specific focus on S100 protein expression as a marker of astroglial activation. Methods: Twenty-four male Sprague-Dawley rats were randomly assigned to three groups (n=8): Control, TBI, and TBI + Nebivolol. TBI was induced via the weight-drop method (50 g/m). Nebivolol (10 mg/kg/day) was administered orally for 14 days. Hippocampal tissues were harvested on day 14 for hematoxylin-eosin (H&E) and S100 immunohistochemical analyses. Statistical evaluation was performed using one-way ANOVA or Kruskal-Wallis tests (p<0.05). Results: The TBI group exhibited neuronal degeneration, nuclear pyknosis, vascular dilation, and disrupted cytoarchitecture, along with intense S100 expression in neurons and glial cells. Nebivolol treatment markedly preserved neuronal morphology, reduced vascular alterations, and decreased S100 immunoreactivity, indicating attenuated astrocytic activation. Conclusion: Nebivolol exhibited a therapeutic effect on hippocampal injury after TBI by attenuating structural deterioration and suppressing astroglial activation. These findings indicate that nebivolol may modulate secondary injury processes; however, further molecular and behavioral studies are required to clarify the underlying mechanisms.