Protective effects of sanggenon C against acetaminophen-induced hepatotoxicity via modulation of oxidative stress and inflammation

The present study evaluated the protective effects of sanggenon C against acetaminophen-induced hepatotoxicity in rats through oxidative, inflammatory, biochemical, and histopathological parameters. Twenty-eight male Sprague Dawley rats were divided into four groups: control, acetaminophen (AAP; 0.5 g/kg), sanggenon C (SANG; 0.1 mg/kg), and therapeutic group (AAP+SANG), in which sanggenon C was administered 4 h after acetaminophen exposure. Serum AST, ALT, ALP, LDH, and CK activities were determined. Oxidative stress and antioxidant status were assessed by measuring MDA, GSH, NO, TAS, and TOS levels in blood and liver tissue. Inflammatory responses were evaluated by determining TNF-α, IL-1β, IL-6, IFN-γ, COX-2, PGE₂, and NF-κB levels. Liver tissue was also examined histopathologically. Acetaminophen administration caused significant hepatic injury, characterized by increased transaminase and LDH activities, elevated oxidative stress, enhanced inflammatory mediator levels, and marked histopathological alterations. Sanggenon C treatment reduced lipid peroxidation, improved antioxidant status, modulated inflammatory responses, and attenuated structural liver damage. These findings suggest that sanggenon C mitigates acetaminophen-induced hepatotoxicity by regulating oxidative stress and inflammatory pathways and may have potential as a natural hepatoprotective agent.