Tasimelteon Attenuates Lung Injury Following Traumatic Brain Injury: Histopathological and Immunohistochemical Evidence in a Rat Model

ObjectiveTraumatic 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 MethodForty 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-α).ResultsTBI induced significant alveolar damage, hyperemia, edema, and elevated Bax and TNF-α expression while reducing anti-apoptotic Bcl-2 levels. TASI, particularly at 10 mg/kg, significantly reversed these histological and molecular alterations (p < 0.05).ConclusionTASI 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.