Trilobatin Possesses Protective Potentials on H₂O₂-Induced HepG2 Cells by Suppressing Oxidative Stress: Involvement of Nrf2/Keap1 Signal Pathway

Abstract

Trilobatin, a natural dihydrochalcone compound, possesses various biological activities. However, few investigations have been carried out on the mechanisms of trilobatin against oxidative stress. To comprehend the effects and mechanism of trilobatin on oxidative stress after hepatic injury, H₂O₂-induced HepG2 cells were used in this research. The results indicated that trilobatin enhanced the viability and improved the apoptosis morphology of HepG2 cells induced by H₂O₂. The decrease of Mitochondrial Membrane Potential (MMP) and the increase of the antioxidant-related enzymes involving Superoxide Dismutase (SOD), Glutathione Peroxidase (GSH-Px), and Catalase (CAT), as well as the reduced levels of alanine Aminotransferase (ALT) and aspartate Aminotransferase (AST), could be responsible for the protective effect of trilobatin on H₂O₂-induced HepG2 cells. Furthermore, the Nuclear erythroid-2 Related Factor 2 (Nrf2)/Kelch-like ECH Associated Protein-1 (Keap-1) pathway was activated by trilobatin in H₂O₂-induced HepG2 cells. These results indicated that trilobatin has a strong protective capacity on H₂O₂-induced HepG2 cells by inhibiting oxidative stress via Nrf2/Keap1 signaling pathway. This research implies that trilobatin might be a useful antioxidant used to prevent liver diseases caused by oxidative stress.