Eugenol protects human liver HepG2 cells from H₂O₂-induced oxidative hepatotoxicity by maintaining ROS homeostasis, increasing IL-10 level, and upregulating CYP1B1 gene expression

Liver injury occurs due to continuous exposure to chemical or biological hazards. Eugenol (EUG), a phenolic compound derived from red betel (Piper crocatum) leaves, has multivalent effects, primarily on antioxidant and antibacterial applications. The conducted research sought to investigate the safeguarding activities of EUG on hydrogen peroxide (H₂O₂)-induced toxicity of human liver HepG2 cells by examining homeostasis, interleukin 10 (IL-10), malondialdehyde (MDA) levels, reactive oxygen species (ROS) level and cytochrome P450 family 1 subfamily B member 1 (CYP1B1) gene expression. The H₂O₂-induced hepatotoxic cells, which served as a positive control, were treated with EUG. The measurements for IL-10 and MDA levels were made using enzyme-linked immunosorbent assay (ELISA), flow cytometry was employed for ROS level, and reverse transcription-quantitative real-time PCR (RT-qPCR) was used for CYP1B1 gene expression assay. EUG 6.25; 25 μg/mL increased IL-10 levels at 55.33 and 47.52 pg/mL compared to the positive control at 21.66 pg/mL. EUG 6.25; 25 μg/mL lowered MDA levels at 679.07 and 651.60 ng/mL compared to the positive control at 845.33 μg/mL. EUG 6.25; 25 μg/mL suppressed ROS level at 15.83 and 19.40% compared to the positive control at 24.10%. EUG 6.25; 25 μg/mL also up-regulated CYP1B1 gene expression. In conclusion, EUG exhibited excellent hepatoprotective effects in hepatotoxic cells model by maintaining ROS homeostasis, increasing IL-10, decreasing MDA levels, and upregulating CYP1B1 gene expression.