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Endoplasmic reticulum stress induced by an ethanol extract of Coicis semen in Chang liver cells

BACKGROUND: It is well known that endoplasmic reticulum (ER) stress plays a huge role in development of metabolic diseases. Specially, ER stress-induced cellular dysfunction has a significant involvement in the pathogenesis of human chronic disorders. This study was designed to study to assess wheth...

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Detalles Bibliográficos
Autores principales: Kim, Hwa Yeon, Song, Ha Na, Davaatseren, Munkhtugs, Chang, Hyun Joo, Chun, Hyang Sook
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5859727/
https://www.ncbi.nlm.nih.gov/pubmed/29554897
http://dx.doi.org/10.1186/s12906-018-2175-z
Descripción
Sumario:BACKGROUND: It is well known that endoplasmic reticulum (ER) stress plays a huge role in development of metabolic diseases. Specially, ER stress-induced cellular dysfunction has a significant involvement in the pathogenesis of human chronic disorders. This study was designed to study to assess whether an ethanol extract of Coicis Semen (CSE) and coixol induces the ER stress in Chang liver cells. METHODS: Coicis Semen was mixed with 95% ethanol at a ratio of 1:10 (w/v) and freeze dried. Chang liver cells were seeded to 96-well plates and treated with or without CSE (100, 200, 300, 500, or 1000 μg/mL) or coixol (100, 200, 300, 500, 750, or 1000 μg/mL). cell viability was analyzed with MTT assay. Effects of CSE and coixol on expression of the genes for ER stress markers were determined with qRT-PCR and the expression of the protein levels of ER stress markers were determined with western blotting. RESULTS: The concentration causing 50% inhibition (IC(50)) for CSE and coixol was 250 and 350 μg/mL, respectively. The CSE and coixol increased the gene expression of BiP and CHOP in a dose-dependent manner. Furthermore, CSE and coixol dose-dependently increased the the expression of XBP1. CONCLUSIONS: CSE or coixol may have cytotoxic effect to Chang liver cells and, may induce ER stress and stimulate the UPR via activation of the PERK and IRE1 pathways in normal liver cells. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12906-018-2175-z) contains supplementary material, which is available to authorized users.