Protective effects of chebulic acid from Terminalia chebula Retz. against t-BHP-induced oxidative stress by modulations of Nrf2 and its related enzymes in HepG2 cells.
Hye-Lim JungSung-Yong YangMin Cheol PyoChung-Oui HongMi-Hyun NamJin-Won LeeKwang-Won LeePublished in: Food science and biotechnology (2018)
Although chebulic acid isolated from Terminalia chebular has diverse biological effects, its effects on the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the expression of downstream genes have not been elucidated. The purpose of this research is to investigate the hepatoprotective mechanism of chebulic acid against oxidative stress produced by tert-butyl hydroperoxide (t-BHP) in liver cells. The treatment with chebulic acid attenuated cell death in t-BHP-induced HepG2 liver cells and increased intracellular glutathione content, upregulated the activity of heme oxygenase-1, and also increased the translocation of Nrf2 into the nucleus and Nrf2 target gene expression in a dose-dependent manner. The exposure of chebulic acid activated the phosphorylation of mitogen-activated protein kinases. The overall result is that chebulic acid has cytoprotective effect on t-BHP-induced hepatotoxicity in HepG2 cells through Nrf2-mediated antioxidant enzymes.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- gene expression
- cell death
- nuclear factor
- cell cycle arrest
- poor prognosis
- drug induced
- dna damage
- high glucose
- dna methylation
- signaling pathway
- endothelial cells
- nitric oxide
- inflammatory response
- endoplasmic reticulum stress
- genome wide
- hydrogen peroxide
- immune response
- reactive oxygen species
- bioinformatics analysis