scholarly journals Free fatty acid-induced histone acetyltransferase activity accelerates lipid accumulation in HepG2 cells

2019 ◽  
Vol 13 (3) ◽  
pp. 196 ◽  
Author(s):  
Sangwon Chung ◽  
Jin-Taek Hwang ◽  
Jae Ho Park ◽  
Hyo-Kyoung Choi
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Histone Acetyltransferase ◽  
Acetyltransferase Activity ◽  
Histone Acetyltransferase Activity

scholarly journals Activation of free fatty acid receptor 1 improves hepatic steatosis through a p38-dependent pathway

2014 ◽  
Vol 53 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Horng-Yih Ou ◽  
Hung-Tsung Wu ◽  
Feng-Hwa Lu ◽  
Yu-Chu Su ◽  
Hao-Chang Hung ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Hepatic Steatosis ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Acid Receptor ◽  
Hepatic Lipid Accumulation ◽  
Free Fatty Acid Receptor ◽  
Related Proteins ◽  
Dependent Pathway

Hepatic steatosis is highly correlated with insulin resistance and diabetes. Although, it has been demonstrated that activation of free fatty acid receptor 1 (FFAR1) by agonists showed benefits for the improvement of diabetes, the effects of FFAR1 agonists on hepatic steatosis were unknown. In this study, a high fat diet (HFD)-induced hepatic steatosis animal model was utilized to evaluate the effects of an FFAR1 agonist, GW9508, on hepatic lipid accumulation, and HepG2 hepatoma cells were also used to clarify the possible mechanisms. Administration of GW9508 significantly decreased the hepatic lipid accumulation with decreased expressions of lipogenesis-related proteins in HFD mice. Knockdown of hepaticFfar1by lentiviral vectors containing short hairpin RNA targeted toFfar1diminished the effect of GW9508 in HFD mice. In addition, GW9508 decreased oleic acid-induced lipid accumulation in HepG2 cells by decreases in the expression of lipogenesis-related proteins. Moreover, GW9508 downregulated the expression of sterol regulatory element-binding protein 1 (SREBP1) through a p38-dependent pathway, whereas knockdown ofFfar1in HepG2 cells diminished the effect of GW9508 on the decrease in SREBP1. Considering all these results together, GW9508 exerts a therapeutic effect to improve hepatic steatosis through a p38-dependent pathway. Thus, investigation of chemicals that act on FFAR1 might be a new strategy for the treatment of hepatic steatosis.

Assays of nucleosome assembly and the inhibition of histone acetyltransferase activity. (5) Preparation of core histones

2007 ◽  
Author(s):  
Takahito Yamasaki ◽  
Takehide Murata ◽  
Chunyuan Jin ◽  
Kohsuke Kato ◽  
Michiya Noguchi ◽  
...  
Keyword(s):  
Histone Acetyltransferase ◽  
Nucleosome Assembly ◽  
Acetyltransferase Activity ◽  
Core Histones ◽  
Histone Acetyltransferase Activity

scholarly journals Aqueous Extract of Pepino Leaves Ameliorates Palmitic Acid-Induced Hepatocellular Lipotoxicity via Inhibition of Endoplasmic Reticulum Stress and Apoptosis

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 903
Author(s):  
Jen-Ying Hsu ◽  
Hui-Hsuan Lin ◽  
Charng-Cherng Chyau ◽  
Zhi-Hong Wang ◽  
Jing-Hsien Chen
Keyword(s):  
Fatty Acid ◽  
Palmitic Acid ◽  
Er Stress ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Target Genes ◽  
Liver Lipid ◽  
Antioxidant Response ◽  
Long Chain Fatty Acid ◽  
Nrf2 Expression

Saturated fatty acid is one of the important nutrients, but contributes to lipotoxicity in the liver, causing hepatic steatosis. Aqueous pepino leaf extract (AEPL) in the previous study revealed alleviated liver lipid accumulation in metabolic syndrome mice. The study aimed to investigate the mechanism of AEPL on saturated long-chain fatty acid-induced lipotoxicity in HepG2 cells. Moreover, the phytochemical composition of AEPL was identified in the present study. HepG2 cells treated with palmitic acid (PA) were used for exploring the effect of AEPL on lipid accumulation, apoptosis, ER stress, and antioxidant response. The chemical composition of AEPL was analyzed by HPLC-ESI-MS/MS. AEPL treatment reduced PA-induced ROS production and lipid accumulation. Further molecular results revealed that AEPL restored cytochrome c in mitochondria and decreased caspase 3 activity to cease apoptosis. In addition, AEPL in PA-stressed HepG2 cells significantly reduced the ER stress and suppressed SREBP-1 activation for decreasing lipogenesis. For defending PA-induced oxidative stress, AEPL promoted Nrf2 expression and its target genes, SOD1 and GPX3, expressions. The present study suggested that AEPL protected from PA-induced lipotoxicity through reducing ER stress, increasing antioxidant ability, and inhibiting apoptosis. The efficacy of AEPL on lipotoxicity was probably concerned with kaempferol and isorhamnetin derived compounds.

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