Ali Serdar OGUZOGLU, Musa CANAN, Furkan Cagri OGUZLAR, Halil ASCI, Ozlem OZMEN
Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi - 2026;33(2):114-121
Objective: Traumatic brain injury (TBI) frequently causes secondary damage in distant organs, particularly the lungs, contributing to poor clinical outcomes. We aimed to assess whether tasimelteon (TASI), a melatonin receptor agonist, could mitigate pulmonary injury resulting from TBI in a rat model. Material and Method: Forty male Wistar albino rats were randomly allocated to four distinct experimental groups: control, trauma (TRA), TRA + TASI 1mg/kg, and TRA + TASI 10mg/kg. TBI was induced via Marmarou's weight-drop model. Lung tissue samples were evaluated 24 hours after TBI via histopathological and immunohistochemical analyses targeting B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and Tumor Necrosis Factor-alpha (TNF-alpha). Results: TBI induced significant alveolar damage, hyperemia, edema, and elevated Bax and TNF-alpha expression while reducing anti-apoptotic Bcl-2 levels. TASI, particularly at 10 mg/kg, significantly reversed these histological and molecular alterations (p < 0.05). Conclusion: TASI provides dose-dependent protection against TBI-induced lung injury through modulation of apoptotic and inflammatory pathways. Its melatoninergic actions may represent a promising therapeutic option for managing multi-organ complications post-TBI.
