scholarly journals Zanthoxylum ailanthoides Suppresses Oleic Acid-Induced Lipid Accumulation through an Activation of LKB1/AMPK Pathway in HepG2 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Eun-Bin Kwon ◽  
Myung-Ji Kang ◽  
Soo-Yeon Kim ◽  
Yong-Moon Lee ◽  
Mi-Kyeong Lee ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Methanol Extract ◽  
De Novo ◽  
Oxygen Species ◽  
Gene Expressions ◽  
Intracellular Lipid ◽  
Ampk Signaling ◽  
Intracellular Lipid Accumulation

Zanthoxylum ailanthoides (ZA) has been used as folk medicines in East Asian and recently reported to have several bioactivity; however, the studies of ZA on the regulation of triacylglycerol (TG) biosynthesis have not been elucidated yet. In this study, we examined whether the methanol extract of ZA (ZA-M) could reduce oleic acid- (OA-) induced intracellular lipid accumulation and confirmed its mode of action in HepG2 cells. ZA-M was shown to promote the phosphorylation of AMPK and its upstream LKB1, followed by reduction of lipogenic gene expressions. As a result, treatment of ZA-M blocked de novo TG biosynthesis and subsequently mitigated intracellular neutral lipid accumulation in HepG2 cells. ZA-M also inhibited OA-induced production of reactive oxygen species (ROS) and TNF-α, suggesting that ZA-M possess the anti-inflammatory feature in fatty acid over accumulated condition. Taken together, these results suggest that ZA-M attenuates OA-induced lipid accumulation and inflammation through the activation of LKB1/AMPK signaling pathway in HepG2 cells.

scholarly journals microRNA-99a Restricts Replication of Hepatitis C Virus by Targeting mTOR and De Novo Lipogenesis

Viruses ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 696 ◽  
Author(s):  
Eun Byul Lee ◽  
Pil Soo Sung ◽  
Jung-Hee Kim ◽  
Dong Jun Park ◽  
Wonhee Hur ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Lipid Accumulation ◽  
De Novo ◽  
Regulatory Element ◽  
Mammalian Target Of Rapamycin ◽  
De Novo Lipogenesis ◽  
Hcv Rna ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

In this study, we investigated the role of microRNA-99a (miR-99a) in hepatitis C virus (HCV) replication and lipogenesis in hepatocytes. Cell-culture-derived HCV (HCVcc) infection caused down-regulation of miR-99a in Huh-7 cells, and the relative levels of miR-99a were significantly lower in the sera of the HCV-infected patients than in those of healthy controls. Transfection of miR-99a-5p mimics resulted in a decrease in the intracellular and secreted HCV RNA levels. It also caused a decreased mammalian target of rapamycin (mTOR) protein level and phosphorylation of its downstream targets in HCV-replicating cells. Sterol regulatory element binding protein (SREBP)-1c expression and intracellular lipid accumulation decreased when either miR-99a-5p mimics or si-mTOR was transfected in oleic acid-treated Huh-7 cells. Overexpression of mTOR rescued HCV RNA replication and lipid droplet accumulation in miR-99a-5p mimics-transfected HCV replicon cells. Our data demonstrated that miR-99a ameliorates intracellular lipid accumulation by regulating mTOR/SREBP-1c and causes inefficient replication and packaging of intracellular HCV.

scholarly journals Maternal Diabetes Leads to Unphysiological High Lipid Accumulation in Rabbit Preimplantation Embryos

Endocrinology ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 1498-1509 ◽  
Author(s):  
Maria Schindler ◽  
Mareike Pendzialek ◽  
Alexander Navarrete Santos ◽  
Torsten Plösch ◽  
Stefanie Seyring ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Accumulation ◽  
Fatty Acid Synthase ◽  
De Novo ◽  
Binding Protein ◽  
Maternal Diabetes ◽  
Preimplantation Embryos ◽  
Intracellular Lipid ◽  
Fatty Acid Binding ◽  
Intracellular Lipid Accumulation

According to the “developmental origin of health and disease” hypothesis, the metabolic set points of glucose and lipid metabolism are determined prenatally. In the case of a diabetic pregnancy, the embryo is exposed to higher glucose and lipid concentrations as early as during preimplantation development. We used the rabbit to study the effect of maternal diabetes type 1 on lipid accumulation and expression of lipogenic markers in preimplantation blastocysts. Accompanied by elevated triglyceride and glucose levels in the maternal blood, embryos from diabetic rabbits showed a massive intracellular lipid accumulation and increased expression of fatty acid transporter 4, fatty acid–binding protein 4, perilipin/adipophilin, and maturation of sterol-regulated element binding protein. However, expression of fatty acid synthase, a key enzyme for de novo synthesis of fatty acids, was not altered in vivo. During a short time in vitro culture of rabbit blastocysts, the accumulation of lipid droplets and expression of lipogenic markers were directly correlated with increasing glucose concentration, indicating that hyperglycemia leads to increased lipogenesis in the preimplantation embryo. Our study shows the decisive effect of glucose as the determining factor for fatty acid metabolism and intracellular lipid accumulation in preimplantation embryos.

scholarly journals Molecular mechanism of intracellular lipid accumulation: Suppressive effect of PycnogenolR in liver cells

2013 ◽  
Vol 3 (9) ◽  
pp. 353 ◽  
Author(s):  
Shoichiro Ikuyama ◽  
Bin Fan ◽  
Jian-Qiu Gu ◽  
Kumiko Mukae ◽  
Hideyuki Watanabe
Keyword(s):  
Oleic Acid ◽  
Fatty Liver ◽  
Lipid Accumulation ◽  
Promoter Activity ◽  
Pathological Condition ◽  
Suppressive Effect ◽  
Liver Cells ◽  
Intracellular Lipid ◽  
Target Molecule ◽  
Intracellular Lipid Accumulation

Cells are physiologically ready to accumulate lipids such as triacylglycerides in the cytoplasm. Five classes of perilipin (PLIN) family proteins are known to be involved in the process of intracellular lipid accumulation. PLIN2 is expressed ubiquitously including adipocytes, hepatocytes and macrophages. Over-expression of PLIN2 is demonstrated in the lesions of fatty liver diseases and atherosclerosis. Suppression of PLIN2 expression prevents from developing these pathological conditions in animal models, suggesting that PLIN2 could be a therapeutic target molecule for excessive intracellular lipid accumulation which leads to various metabolic derangements. The PLIN2 gene promoter has two important cis-acting elements in close proximity:AP-1 element which mediates inflammatory signals and PPRE which mediates free fatty acid effect. In NMuLi mouse liver cells, FFA such as oleic acid requires both functional AP-1 and PPRE simultaneously to stimulate the promoter activity, indicating the presence of intimate interaction of inflammatory and metabolic signals on this gene. PycnogenolR, French maritime pine bark extracts, suppressed the oleic acid-induced PLIN2 expression and lipid accumulation in NMuLi cells. We found that PycnogenolR did not suppress the PLIN2 promoter activity or AP-1 binding to DNA. Instead, PycnogenolR facilitates the PLIN2 mRNA degradation, leading to suppression of lipid accumulation. This effect seems to be independent of antioxidant effect of PycnogenolR. We raise the idea that PLIN2 is a putative target molecule for prevention of pathological condition induced by excessive lipid accumulation, and this class of natural compounds could be putative therapeutic modalities.Key words: PycnogenolR, lipid droplet, perilipin, fatty liver disease

S-petasin inhibits lipid accumulation in oleic acid-induced HepG2 cells through activation of the AMPK signaling pathway

2020 ◽  
Vol 11 (6) ◽  
pp. 5664-5673 ◽  
Author(s):  
Lu Guo ◽  
Jum Soon Kang ◽  
Young Hoon Park ◽  
Beong Il Je ◽  
Yong Jae Lee ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Signaling Pathway ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Ampk Signaling

S-petasin inhibits lipid accumulation in oleic acid-induced HepG2 cells.

scholarly journals Inhibitory Activity of Intracellular Lipid Accumulation by Various Marine Extracts in HepG2 Cells

2012 ◽  
Vol 44 (3) ◽  
pp. 362-366 ◽  
Author(s):  
Byoung-Mok Kim ◽  
Ji-Hee Jung ◽  
Dong-Soo Kim ◽  
Young-Myoung Kim ◽  
In-Hak Jeong
Keyword(s):  
Inhibitory Activity ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

scholarly journals Posidonia oceanica (L.) Delile Extract Reduces Lipid Accumulation through Autophagy Activation in HepG2 Cells

2021 ◽  
Vol 14 (10) ◽  
pp. 969
Author(s):  
Marzia Vasarri ◽  
Emanuela Barletta ◽  
Donatella Degl’Innocenti
Keyword(s):  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Posidonia Oceanica ◽  
Intracellular Lipid ◽  
Alcoholic Fatty Liver ◽  
Ribosomal Protein S6 ◽  
Intracellular Lipid Accumulation ◽  
Human Hepatoma Hepg2 Cells ◽  
Lipid Reduction ◽  
The Relationship

Posidonia oceanica (L.) Delile is a marine plant traditionally used as an herbal medicine for various health disorders. P. oceanica leaf extract (POE) has been shown to be a phytocomplex with cell-safe bioactivities, including the ability to trigger autophagy. Autophagy is a key pathway to counteract non-alcoholic fatty liver disease (NAFLD) by controlling the breakdown of lipid droplets in the liver. The aim of this study was to explore the ability of POE to trigger autophagy and reduce lipid accumulation in human hepatoma (HepG2) cells and then verify the possible link between the effect of POE on lipid reduction and autophagy activation. Expression levels of autophagy markers were monitored by the Western blot technique in POE-treated HepG2 cells, whereas the extent of lipid accumulation in HepG2 cells was assessed by Oil red O staining. Chloroquine (CQ), an autophagy inhibitor, was used to study the relationship between POE-induced autophagy and intracellular lipid accumulation. POE was found to stimulate an autophagy flux over time in HepG2 cells by lowering the phosphorylation state of ribosomal protein S6, increasing Beclin-1 and LC3-II levels, and decreasing p62 levels. By blocking autophagy with CQ, the effect of POE on intracellular lipid accumulation was clearly reversed, suggesting that the POE phytocomplex may reduce lipid accumulation in HepG2 cells by activating the autophagic process. This work indicates that P. oceanica may be considered as a promising molecule supplier to discover new natural approaches for the management of NAFLD.

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