AI Summary & Key Takeaways
AI InsightAMA treatment was associated with reduced histopathological alterations and lower immunoreactivity of pro-inflammatory cytokines compared with the untreated trauma group.
📌 3 Key Takeaways
Abstract
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-α), interleukin 6 (IL-6), and interferon beta (IFN-β). Results TBI significantly elevated hepatic expression of pro-inflammatory cytokines (IFN-β, IL-6, TNF-α) 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.
Özet
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-α), interleukin 6 (IL-6), and interferon beta (IFN-β). Results TBI significantly elevated hepatic expression of pro-inflammatory cytokines (IFN-β, IL-6, TNF-α) 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.