Abstract
ABSTRACTThe present study aimed to investigate the protective effects of selenium (SE) against enrofloxacin (ENRO) induced liver damage through oxidative stress, inflammation, and autophagy pathways. Rats were divided into four groups: control (received physiological saline via oral gavage and intraperitoneal (i.p.) injection for 7 days); selenium (1 mg/kg, oral, 7 days); enrofloxacin (150 mg/kg, i.p., 7 days); and enrofloxacin (150 mg/kg, i.p., 7 days) + selenium (1 mg/kg, oral, 7 days). In liver tissues, oxidative stress markers including malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured. Additionally, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and Beclin-1 expression were analyzed to evaluate inflammatory and autophagic responses ENRO administration increased NF-κB, IL-1β, TNF-α, and Beclin-1 expression together with elevated MDA levels, while decreasing GSH levels and SOD, CAT, and GPx activities. These alterations indicate increased lipid peroxidation, inflammation, and autophagy. These findings indicate that ENRO disrupts antioxidant defense systems and promotes inflammatory and autophagy-related responses in liver tissue. SE supplementation reduced MDA levels, enhanced GSH levels and antioxidant enzyme activities, and significantly ameliorated these alterations by suppressing NF-κB, IL-1β, TNF-α, and Beclin-1 expression. In conclusion, SE was found to exert hepatoprotective effects against ENRO induced liver injury by reducing lipid peroxidation, strengthening antioxidant defense systems, and regulating inflammatory and autophagic responses.