Liquiritigenin prevents palmitate-induced beta-cell apoptosis via estrogen receptor-mediated AKT activation
- Authors
- Bae, Gong Deuk; Park, Eun-Young; Baek, Dong Jae; Jun, Hee-Sook; Oh, Yoon Sin
- Issue Date
- May-2018
- Publisher
- ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
- Keywords
- Liquiritigenin; Beta-cell; Apoptosis; Endoplasmic reticulum stress; AKT
- Citation
- BIOMEDICINE & PHARMACOTHERAPY, v.101, pp.348 - 354
- Journal Title
- BIOMEDICINE & PHARMACOTHERAPY
- Volume
- 101
- Start Page
- 348
- End Page
- 354
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3843
- DOI
- 10.1016/j.biopha.2018.02.097
- ISSN
- 0753-3322
- Abstract
- Liquiritigenin (LQ) is a major active component of licorice root, which is a flavone used for treating many diseases, including diabetes. LQ has been shown to exhibit a glucose-lowering effect in diabetic mice. Therefore, we investigated the potential of LQ to protect against lipotoxicity-induced beta-cell apoptosis and the underlying molecular mechanisms. Exposure of INS-1 rat insulinoma cells to LQ significantly increased cell viability and blocked palmitate (PA)-induced apoptosis, as evidenced by the reduction of Annexin-V-stained cells, cleaved caspase-3 levels, and poly (ADP-ribose) polymerase (PARP) activity, as well as upregulation of Bcl-2 expression. Moreover, LQ treatment significantly reduced the endoplasmic reticulum (ER) stress response by reducing phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eIF-2a, and CHOP expression in PA-treated INS-1 cells. The anti-apoptotic effect of LQ treatment was reversed through co-treatment with fulvestrant, a specific inhibitor of the estrogen receptor. LQ also increased AKT phosphorylation, and inactivation of this molecular event failed to decrease PERK phosphorylation with LQ treatment in PA-treated INS-1 cells. This effect was further accompanied by an inability to recover cell viability. These results suggest that LQ protects INS-1 cells from lipotoxicity-induced apoptosis by suppressing ER stress. We conclude that estrogen receptor-mediated AKT phosphorylation is one of the mechanisms contributing to the anti-apoptotic effect of LQ.
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