Trilobatin Possesses Protective Potentials on H2O2-Induced HepG2 Cells by Suppressing Oxidative Stress: Involvement of Nrf2/Keap1 Signal Pathway
- 1 Department of Food Science and Engineering, Colin Ratledge Center for Microbial Lipids, School of Agricultural Engineering and Food Science, Shandong University of Technology, Zibo, China
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.
DOI: https://doi.org/10.3844/ajbbsp.2023.336.346
Copyright: © 2023 Yuhan Zhai, Yuqing Zhang, Yaping Li, Ming He, Shaoxuan Yu, Haifang Xiao and Yuanda Song. This is an open access article distributed under the terms of the
Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Keywords
- Trilobatin
- Oxidative Stress
- HepG2 Cell
- Nrf2/Keap-1