Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells
- Authors
- Jung, Tae Woo; Hwang, Hwan-Jin; Hong, Ho Cheol; Choi, Hae Yoon; Yoo, Hye Jin; Baik, Sei Hyun; Choi, Kyung Mook
- Issue Date
- 25-6월-2014
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Non-alcoholic fatty liver; Resolvin D1; c-Jun N-terminal kinase; Proliferator-activated receptor-gamma; ER stress
- Citation
- MOLECULAR AND CELLULAR ENDOCRINOLOGY, v.391, no.1-2, pp.30 - 40
- Indexed
- SCIE
SCOPUS
- Journal Title
- MOLECULAR AND CELLULAR ENDOCRINOLOGY
- Volume
- 391
- Number
- 1-2
- Start Page
- 30
- End Page
- 40
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/98198
- DOI
- 10.1016/j.mce.2014.04.012
- ISSN
- 0303-7207
- Abstract
- Research has indicated that stress on the endoplasmic reticulum (ER) of a cell affects the pathogenesis of metabolic disorders such as obesity, type 2 diabetes mellitus, and non-alcoholic fatty liver disease (NAFLD). Resolvins, a novel family derived from omega-3 polyunsaturated fatty acids, have anti-inflammatory and insulin sensitizing properties, and it has been suggested that they play a role in the amelioration of obesity-related metabolic dysfunctions. This study showed that pretreatment with resolvin D1 (RvD1) attenuated ER stress-induced apoptosis and also decreased caspase 3 activity in HepG2 cells. Furthermore, RvD1 significantly decreased tunicamycin-induced triglycerides accumulation as well as SREBP1 expression. However, tunicamycin-induced ER stress markers were not significantly affected by RvD1 treatment. Moreover, RvD1 treatment did not affect the tunicamycin-induced expression of chaperones that assist protein folding in the ER. These results suggest that RvD1-conferred cellular protection may occur downstream of the ER stress. This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected. In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. In conclusion, RvD1 attenuated ER stress-induced hepatic steatosis and apoptosis via the JNK-mediated pathway. This study may provide insight into a novel underlying mechanism and a strategy for treating NAFLD. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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