Oxidative Stress and Inflammation Markers in Lipopolysaccharide (LPS)-Induced Acute Kidney Injury in Rats?The Potential Role of Lacosamide
Background: Sepsis is a well-known cause of multiple organ failure although its molecular mechanism is not fully defined. In this study, antioxidant, and anti-inflammatory effects of lacosamide (LCM) on the kidney tissue of rats with sepsis were investigated in the experimental LPS-induced sepsis model. Materials and Methods: Twenty-four female Wistar albino rats were divided into three groups: Control group, LPS group (5 mg/kg LPS, i.p, single dose), and LPS+LCM (5 mg/kg LPS, i.p, single dose + 40 mg/kg LCM, i.p, 3 days pretreatment). Malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activities were analyzed in kidney tissues. Creatinine, blood urea nitrogen (BUN) and uric acid levels were measured in the blood. Hyperemia and micro hemorrhages were examined by histopathological analysis. In addition, TNF-α, C-reactive protein (CRP), IL-1β, heat shock protein-70 (HSP70), and MDA expressions were evaluated. Results: The levels of MDA, BUN, Creatinine, and uric acid were increased, whereas CAT and SOD levels were decreased in LPS group. Histopathological and immunohistochemical examinations of the kidney tissue revealed hyperemia and micro hemorrhages together with an increase in TNF-α, CRP, IL-1β, HSP70, and MDA expressions in LPS group. Pretreatment with LCM prevented the development of all the pathological findings parameters in the kidney and serum. Conclusion: LCM pretreatment decreased oxidative damage in sepsis-induced kidney injury in the experimental model. However, LCM demonstrated favorable properties against sepsis-induced acute kidney injury reducing pro-inflammatory cytokine release.