Emodin exerts protective effect against palmitic acid-induced endoplasmic reticulum stress in HepG2 cells
10.4163/jnh.2019.52.2.176
- Author:
Shalom Sara THOMAS
1
;
Sora PARK
;
Youn Soo CHA
;
Kyung Ah KIM
Author Information
1. Department of Food Science and Human Nutrition, Chonbuk National University, Jeonju, Jeonbuk 54896, Korea.
- Publication Type:Original Article
- Keywords:
emodin;
palmitic acid;
endoplasmic reticulum stress;
sirtuins
- MeSH:
Emodin;
Endoplasmic Reticulum Stress;
Endoplasmic Reticulum;
Hep G2 Cells;
Immunoblotting;
Insurance Benefits;
Palmitic Acid;
Polymerase Chain Reaction;
RNA, Messenger;
Sirtuins;
Unfolded Protein Response
- From:Journal of Nutrition and Health
2019;52(2):176-184
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Protein overloading in the endoplasmic reticulum (ER) leads to endoplasmic reticulum stress, which exacerbates various disease conditions. Emodin, an anthraquinone compound, is known to have several health benefits. The effect of emodin against palmitic acid (PA) - induced ER stress in HepG2 cells was investigated. METHODS: HepG2 cells were treated with varying concentrations of palmitic acid to determine the working concentration that induced ER stress. ER stress associated genes such as ATF4, XBP1s, CHOP and GRP78 were checked using RT- PCR. In addition, the expression levels of unfolded protein response (UPR) associated proteins such as IRE1α, eIF2α and CHOP were checked using immunoblotting to confirm the induction of ER stress. The effect of emodin on ER stress was analyzed by treating HepG2 cells with 750 µM palmitic acid and varying concentrations of emodin, then analyzing the expression of UPR associated genes. RESULTS: It was evident from the mRNA and protein expression results that palmitic acid significantly increased the expression of UPR associated genes and thereby induced ER stress. Subsequent treatment with emodin reduced the mRNA expression of ATF4, GRP78, and XBP1s. Furthermore, the protein levels of p-IRE1α, p-elF2α and CHOP were also reduced by the treatment of emodin. Analysis of sirtuin mRNA expression showed that emodin increased the levels of SIRT4 and SIRT7, indicating a possible role in decreasing the expression of UPR-related genes. CONCLUSION: Altogether, the results suggest that emodin could exert a protective effect against fatty acid-induced ER stress and could be an agent for the management of various ER stress related diseases.
