Jung Hye-Lim, Yang Sung-Yong, Pyo Min Cheol, Hong Chung-Oui, Nam Mi-Hyun, Lee Jin-Won, Lee Kwang-Won
1Department of Biotechnology, College of Life Science and Biotechnology, Korea University, 145 Anam-ro, Seongbuk-gu, Seoul, 02841 Republic of Korea.
2Analytical Method Development Team, Samsung BIOEPIS, Incheon, 21987 Republic of Korea.
Food Sci Biotechnol. 2018 Sep 27;28(2):555-562. doi: 10.1007/s10068-018-0477-z. eCollection 2019 Apr.
Although chebulic acid isolated from 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 -butyl hydroperoxide (-BHP) in liver cells. The treatment with chebulic acid attenuated cell death in -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 -BHP-induced hepatotoxicity in HepG2 cells through Nrf2-mediated antioxidant enzymes.
尽管从[具体来源未给出]中分离出的诃子酸具有多种生物学效应，但其对核因子红细胞2相关因子2（Nrf2）表达及下游基因表达的影响尚未阐明。本研究旨在探讨诃子酸对肝细胞中叔丁基过氧化氢（t-BHP）产生的氧化应激的肝保护机制。诃子酸处理可减轻t-BHP诱导的HepG2肝细胞死亡，增加细胞内谷胱甘肽含量，上调血红素加氧酶-1的活性，并以剂量依赖的方式增加Nrf2向细胞核的转位及Nrf2靶基因表达。诃子酸的暴露激活了丝裂原活化蛋白激酶的磷酸化。总体结果是，诃子酸通过Nrf2介导的抗氧化酶对t-BHP诱导的HepG2细胞肝毒性具有细胞保护作用。
