Oxidative stress plays a critical role in the pathogenesis of hepatic dysfunction through excessive generation of reactive oxygen species (ROS) and impairment of antioxidant defense systems. This study investigated the iin vitro/i antioxidant and cytoprotective effects of Beta vulgaris ethanol extract in a hydrogen peroxide (Hsub2/subOsub2/sub)-induced oxidative stress model using HepG2 cells. Antioxidant potential was first evaluated through 2, 2-Diphenyl-1-picrylhydrazyl (DPPH) and hydrogen peroxide scavenging assays, where the extract demonstrated strong concentration-dependent radical inhibition, achieving 93.14% DPPH scavenging at 600 µg/ml. The extract exhibited IC₅₀ values of 147.41 µg/mL (DPPH) and 297.82 µg/mL (Hsub2/subOsub2/sub), indicating substantial free radical scavenging capacity comparable to ascorbic acid. In the cell-based model, Hsub2/subOsub2/sub exposure significantly increased malondialdehyde (MDA) levels, confirming lipid peroxidation and oxidative injury. Pretreatment with Beta vulgaris extract reduced MDA concentrations in a dose-dependent manner, with optimal protection observed at 600 µg/ml, comparable to the standard antioxidant silymarin. Furthermore, the extract significantly restored intracellular glutathione (GSH) levels and enhanced antioxidant enzyme activities, including catalase (CAT) and superoxide dismutase (SOD), demonstrating improved cellular redox balance. These findings suggest that Beta vulgaris ethanol extract possesses strong antioxidant and cytoprotective properties and may serve as a promising natural therapeutic candidate for mitigating oxidative stress-mediated hepatic damage.
Belema et al. (Thu,) studied this question.
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