Yapay Zeka Hızlı Bakış & Çıkarımlar
AI InsightIts melatoninergic actions may represent a promising therapeutic option for managing multi-organ complications post-TBI.
📌 3 Maddede Bu Makale
Özet
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-α). Results TBI 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). 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.
Abstract
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-α). Results TBI 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). 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.