Abstract / Summary
Abstract Background Obstructive jaundice can progress to hepatic encephalopathy (HE) through systemic toxin accumulation, oxidative stress, and neuroinflammation. Aims This study investigated the neuroprotective and hepatoprotective effects of ellagic acid (EA) in a bile duct ligation (BDL)-induced experimental HE model, focusing on oxidative stress-responsive heme oxygenase-1 (HO-1) alterations. Methods Forty female Wistar rats were divided into Control, Sham, EA, BDL, and BDL + EA groups. EA (25 mg/kg) was administered prophylactically via intraperitoneal (i.p.) injection for 14 days. Cognitive and locomotor performances were assessed using the Novel Object Recognition (NOR) and Open Field tests (OFT). Biochemical analyses evaluated liver enzymes, bilirubin, reduced glutathione (GSH), malondialdehyde (MDA), HO-1, and interleukin-1β (IL-1β) levels in serum, liver, and hippocampal tissues. Results BDL significantly impaired behavioral performance, increased liver enzymes, MDA, HO-1, and IL-1β levels, and depleted GSH levels in all examined tissues (p < 0.05). EA administration significantly improved cognitive and locomotor outcomes, restored antioxidant status, and reduced lipid peroxidation. Furthermore, EA attenuated HO-1 and IL-1β elevations, suggesting attenuation of oxidative stress and inflammatory responses. Conclusions EA exerts hepatoprotective and neuroprotective effects by restoring oxidant-antioxidant balance and suppressing neuroinflammatory responses, suggesting its potential as a therapeutic approach for liver-brain axis dysfunction.