Protective Effects of Amantadine on Secondary Liver Injury Following Traumatic Brain Injury in an Experimental Rat Model

ObjectiveTraumatic brain injury (TBI) is known to trigger systemicinflammatory responses, leading to damage indistant organs such as the liver. Amantadine (AMA),an NMDA receptor antagonist, exhibits both anti-inflammatoryand neuroprotective properties. This studyinvestigated the protective effects of AMA against liverinjury secondary to TBI in a rat model.Material and MethodForty male Wistar albino rats were randomly assignedto four groups: Control, Trauma (TRA), TRA+AMA-1,and TRA+AMA-7. TBI was induced by the Marmarouweight-drop method. AMA (45 mg/kg/day, intraperitoneal)was administered for 1 and 7 days post-TBI.Liver tissues were harvested and evaluated via histopathologicalscoring and immunohistochemical analysisfor tumor necrosis factor alpha (TNF-α), interleukin6 (IL-6), and interferon beta (IFN-β).ResultsTBI significantly elevated hepatic expression ofpro-inflammatory cytokines (IFN-β, IL-6, TNF-α) andcaused marked histological damage, including hyperemia,hemorrhage, inflammation, and necrosis. AMAtreatment markedly reduced these cytokine expressionsand ameliorated histopathological alterations.The TBI+AMA-7 group exhibited substantial recoverycompared to the TBI group, indicating an associationbetween amantadine treatment and reduced histopathologicalliver injury.ConclusionThe trauma group demonstrated significantly higherhistopathological liver injury scores compared withthe control group. AMA treatment was associatedwith reduced histopathological alterations and lowerimmunoreactivity of pro-inflammatory cytokines comparedwith the untreated trauma group.