Journal
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Volume 365, Issue 3, Pages 485-493Publisher
AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS
DOI: 10.1124/jpet.117.246686
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Funding
- National Research Foundation of Korea (NRF) - Ministry of Science, ICT, and Future Planning [2016R1C1B2012674]
- Korea government Ministry of Education [2017R1D1A1B03028892]
- National Research Foundation of Korea [2017R1D1A1B03028892] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Docosahexaenoic acid (DHA) and its bioactive compounds may have suppressive effects on inflammation, endoplasmic reticulum (ER) stress, and insulin resistance. Protectin DX (PDX), a double lipoxygenase product from DHA has shown a suppressive effect on inflammation and insulin resistance. However, the effects of PDX on ER stress and hepatic steatosis have not been elucidated yet. Herein we report that PDX could stimulate the AMP-activated protein kinase (AMPK) phosphorylation, thereby upregulating oxygen-regulated protein 150 (ORP150) expression in a dose-dependent manner. Treatment of HepG2 cells with PDX attenuated the palmitate-induced triglyceride accumulation through regulation of the sterol regulatory element-binding protein 1 (SREBPI)-mediated pathway. To deal with the pharmacological significance in the protective effects of PDX on hepatic steatosis, we performed in vivo experiments. In a mouse model, the PDX administration would alleviate the high-fat diet-induced hepatic steatosis and trigger the hepatic AMPK phosphorylation and ORP150 expression. PDX improved palmitate-induced and HFD-induced impairment of hepatic lipid metabolism and steatosis through suppression of ER stress via an AMPK-ORP150-dependent pathway.
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