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 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 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.

scholarly journals Association of intracellular lipid accumulation in subcutaneous adipocyte precursors and plasma adipokines in bariatric surgery candidates

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Ioana Hristov ◽  
Veronica Mocanu ◽  
Florin Zugun-Eloae ◽  
Luminita Labusca ◽  
Iustina Cretu-Silivestru ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Lipid Accumulation ◽  
Intracellular Lipid ◽  
Intracellular Lipid Accumulation

Dysregulation of low-density lipoprotein receptor contributes to podocyte injuries in diabetic nephropathy

2015 ◽  
Vol 308 (12) ◽  
pp. E1140-E1148 ◽  
Author(s):  
Yang Zhang ◽  
Kun Ling Ma ◽  
Jing Liu ◽  
Yu Wu ◽  
Ze Bo Hu ◽  
...  
Keyword(s):  
High Glucose ◽  
Lipid Accumulation ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Lipoprotein Receptor ◽  
Intracellular Lipid ◽  
Phenotypic Alteration ◽  
Density Lipoprotein Receptor ◽  
Intracellular Lipid Accumulation

Dyslipidemia plays crucial roles in the progression of diabetic nephropathy (DN). This study investigated the effects of high glucose on lipid accumulation in podocytes and explored its underlying mechanisms. Male db/m and db/db mice were fed a normal chow diet for 8 wk. Immortalised mouse podocytes were treated with or without high glucose for 24 h. The changes to the morphology and ultramicrostructures of the kidneys in mice were examined using pathological staining and electron microscopy. Intracellular lipid accumulation was evaluated by Oil Red O staining and a free cholesterol quantitative assay. The expressions of the molecules involved in low-density lipoprotein receptor (LDLr) pathway and podocyte injury were examined using immunofluorescent staining, real-time PCR, and Western blot. There were increased levels of plasma lipid, serum creatinine, and proteinuria in db/db mice compared with db/m mice. Moreover, there was significant mesangial matrix expansion, basement membrane thickening, podocyte foot process effacement, and phenotypic alteration in the db/db group. Additionally, lipid accumulation in the kidneys of db/db mice was increased due to increased protein expressions of LDLr, sterol regulatory element-binding protein (SREBP) cleavage-activating protein, and SREBP-2. These effects were further confirmed by in vitro studies. Interestingly, the treatment with LDLr siRNA inhibited lipid accumulation in podocytes and decreased the protein expression of molecules associated with phenotypic alteration in podocytes. High glucose disrupted LDLr feedback regulation in podocytes, which may cause intracellular lipid accumulation and alteration of podocyte phenotype, thereby accelerating DN progression.

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