Interleukin-27 as a novel player in alleviating hepatic steatosis: Mechanistic insights from an in vitro analysis
- Authors
- Cho, Wonjun; Oh, Heeseung; Abd El-Aty, A.M.; Özten, Ömer; Jeong, Ji Hoon; Jung, Tae Woo
- Issue Date
- Apr-2024
- Publisher
- Elsevier B.V.
- Keywords
- AMPK; Autophagy; ER stress; IL-27; NAFLD; Obesity
- Citation
- Biochemical and Biophysical Research Communications, v.703
- Journal Title
- Biochemical and Biophysical Research Communications
- Volume
- 703
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/72982
- DOI
- 10.1016/j.bbrc.2024.149671
- ISSN
- 0006-291X
1090-2104
- Abstract
- Interleukin-27 (IL-27) is a recently discovered cytokine that has been implicated in inflammatory and metabolic conditions, such as atherosclerosis and insulin resistance. However, the mechanisms by which IL-27 attenuates hepatic lipid accumulation in hyperlipidemic conditions and counteracts endoplasmic reticulum (ER) stress, a known risk factor for impaired hepatic lipid metabolism, have not been elucidated. This in vitro study was designed to examine the effect of IL-27 on hepatic lipid metabolism. The study included the evaluation of lipogenesis-associated proteins and ER stress markers by Western blotting, the determination of hepatic lipid accumulation by Oil Red O staining, and the examination of autophagosome formation by MDC staining. The results showed that IL-27 treatment reduced lipogenic lipid deposition and the expression of ER stress markers in cultured hepatocytes exposed to palmitate. Moreover, treatment with IL-27 suppressed CD36 expression and enhanced fatty acid oxidation in palmitate-treated hepatocytes. The effects of IL-27 on hyperlipidemic hepatocytes were attenuated when adenosine monophosphate-activated protein kinase (AMPK) or 3-methyladenine (3 MA) were inhibited by small interfering RNA (siRNA). These results suggest that IL-27 attenuates hepatic ER stress and fatty acid uptake and stimulates fatty acid oxidation via AMPK/autophagy signaling, thereby alleviating hepatic steatosis. In conclusion, this study identified IL-27 as a promising therapeutic target for nonalcoholic fatty liver disease (NAFLD). © 2024 Elsevier Inc.
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