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Protectin DX ameliorates hepatic steatosis by suppression of endoplasmic reticulum stress via AMPK-induced ORP150 expression.

Protectin DX ameliorates hepatic steatosis by suppression of endoplasmic reticulum stress via AMPK-induced ORP150 expression.
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Jung TW, Kyung EJ, Kim HC, Shin YK, Lee SH, Park ES, Hacimuftuoglu A, Abd El-Aty AM, Jeong JH,


Jung TW, Kyung EJ, Kim HC, Shin YK, Lee SH, Park ES, Hacimuftuoglu A, Abd El-Aty AM, Jeong JH, (click to view)

Jung TW, Kyung EJ, Kim HC, Shin YK, Lee SH, Park ES, Hacimuftuoglu A, Abd El-Aty AM, Jeong JH,

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The Journal of pharmacology and experimental therapeutics 2018 03 23() pii jpet.117.246686
Abstract

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 docosahexaenoic acid (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 have found 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 (SREBP1)-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 (HFD)-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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