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Chinese Journal of Natural Medicines (English Ed.) ; (6): 250-256, 2015.
Article in English | WPRIM | ID: wpr-812150

ABSTRACT

Serum palmitic acid (PA), a type of saturated fatty acid, causes lipid accumulation and induces toxicity in hepatocytes. Ethanol (EtOH) is metabolized by the liver and induces hepatic injury and inflammation. Herein, we analyzed the effects of EtOH on PA-induced lipotoxicity in the liver. Our results indicated that EtOH aggravated PA-induced apoptosis and lipid accumulation in primary rat hepatocytes in dose-dependent manner. EtOH intensified PA-caused endoplasmic reticulum (ER) stress response in vitro and in vivo, and the expressions of CHOP, ATF4, and XBP-1 in nucleus were significantly increased. EtOH also increased PA-caused cleaved caspase-3 in cytoplasm. In wild type and CHOP(-/-) mice treated with EtOH and high fat diet (HFD), EtOH worsened the HFD-induced liver injury and dyslipidemia, while CHOP knockout blocked toxic effects of EtOH and PA. Our study suggested that targeting UPR-signaling pathways is a promising, novel approach to reducing EtOH and saturated fatty acid-induced metabolic complications.


Subject(s)
Animals , Male , Mice , Rats , Activating Transcription Factor 4 , Metabolism , Apoptosis , Caspase 3 , Chemical and Drug Induced Liver Injury , Metabolism , DNA-Binding Proteins , Metabolism , Diet, High-Fat , Dose-Response Relationship, Drug , Dyslipidemias , Metabolism , Endoplasmic Reticulum Stress , Ethanol , Metabolism , Toxicity , Fatty Liver , Metabolism , Gene Knockout Techniques , Hepatocytes , Metabolism , Lipid Metabolism , Liver , Metabolism , Palmitic Acid , Toxicity , Rats, Sprague-Dawley , Regulatory Factor X Transcription Factors , Signal Transduction , Transcription Factor CHOP , Genetics , Metabolism , Transcription Factors , Metabolism , Unfolded Protein Response , X-Box Binding Protein 1
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