Ali Serdar OGUZOGLU, Musa CANAN, Furkan Cagri OGUZLAR, Halil ASCI, Ozlem OZMEN
Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi - 2026;33(3):279-287
Objective: Traumatic brain injury (TBI) is known to trigger systemic inflammatory responses, leading to damage in distant organs such as the liver. Amantadine (AMA), an NMDA receptor antagonist, exhibits both anti-inflammatory and neuroprotective properties. This study investigated the protective effects of AMA against liver injury secondary to TBI in a rat model. Material and Method: Forty male Wistar albino rats were randomly assigned to four groups: Control, Trauma (TRA), TRA+AMA-1, and TRA+AMA-7. TBI was induced by the Marmarou weight-drop method. AMA (45 mg/kg/day, intraperitoneal) was administered for 1 and 7 days post-TBI. Liver tissues were harvested and evaluated via histopathological scoring and immunohistochemical analysis for tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and interferon beta (IFN-beta). Results: TBI significantly elevated hepatic expression of pro-inflammatory cytokines (IFN-beta, IL-6, TNF-alpha) and caused marked histological damage, including hyperemia, hemorrhage, inflammation, and necrosis. AMA treatment markedly reduced these cytokine expressions and ameliorated histopathological alterations. The TBI+AMA-7 group exhibited substantial recovery compared to the TBI group, indicating an association between amantadine treatment and reduced histopathological liver injury. Conclusion: The trauma group demonstrated significantly higher histopathological liver injury scores compared with the control group. AMA treatment was associated with reduced histopathological alterations and lower immunoreactivity of pro-inflammatory cytokines compared with the untreated trauma group.
