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Chebulic Acid against t ‐BHP‐induced effect via Modulations of Nrf2 and Its Related Enzymes in HepG2 cells
Author(s) -
Lee Kwangwon,
Jung HyeLim,
Yang SungYong
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.538.16
Subject(s) - glutathione , reactive oxygen species , antioxidant , mapk/erk pathway , oxidative stress , heme oxygenase , gclm , chemistry , biochemistry , intracellular , gclc , cysteine , kinase , enzyme , downregulation and upregulation , heme , gene
Chebulic acid, phenolic compound isolated from the ripe fruits of Terminalia chebular Retz. shows diverse biological effects. The purpose of this study is to investigate protective effects of chebulic acid against tert ‐butyl hydroperoxide ( t ‐BHP) induced oxidative stress and its mechanism related to Nrf2 signal pathway in HepG2 cells. Chebulic acid attenuated cell death and production of reactive oxygen species in t ‐BHP‐induced HepG2 cells and increased intracellular glutathione (GSH) content and the ratio of GSH to glutathione disulfide (GSSG). Chebulic acid also upregulated the activity of heme oxygenase‐1 (HO‐1). The treatment with chebulic acid increased the translocation of Nrf2 into the nucleus and the expression of Nrf2 target genes such as γ‐glutamate cysteine ligase and HO‐1 in a dose‐dependent manner. In addition, the exposure of chebulic acid enhanced the phosphorylation of mitogen‐activated protein kinases (MAPK). The overall result is that chebulic acid has cytoprotective effect on t ‐BHP‐induced hepatotoxicity in HepG2 cells through Nrf2‐mediated antioxidant enzymes and MAPK. Support or Funding Information This work was supported by a Grant from the Institute of Life Science and Natural Resources, Korea University. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .