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 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 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 Honokiol Attenuates Lipotoxicity in Hepatocytes via Activating SIRT3-AMPK Mediated Lipophagy

2021 ◽  
Author(s):  
Zhang Tian ◽  
Jingxin Liu ◽  
Jianzhong Zhu ◽  
Rongsong Li ◽  
Ligen Lin
Keyword(s):  
Lipid Accumulation ◽  
Energy Homeostasis ◽  
Nile Red ◽  
Acid Mixture ◽  
Amino Acid Residues ◽  
Alcoholic Fatty Liver ◽  
Docking Analysis ◽  
Chain Acyl ◽  
Intracellular Lipid Accumulation ◽  
Amp Activated Protein Kinase

Abstract Background: Non-alcoholic fatty liver disease (NAFLD) is characterized by ectopic accumulation of triglycerides in the liver. Emerging evidence has demonstrated that lipophagy regulates lipid mobilization and energy homeostasis in liver. Sirtuin 3 (SIRT3), a mitochondrial NAD+-dependent deacetylase, modulates the activities of several substrates involving in autophagy and energy metabolism. Honokiol (HK) is a natural lignan from the plants of Magnolia genus that exhibits potent liver protective property. Methods: AML12 was challenged with 500 μM palmitic acid and 250 μM oleic acid mixture solution to induce lipotoxicity. The expression of autophagy-related and AMP-activated protein kinase (AMPK) pathway proteins was evaluated by Western blotting and immunofluorescence staining. Intracellular lipid accumulation was validated by Nile red staining. Molecular docking analysis was performed on AutoDock 4.2.Results: HK (5 and 10 μM) was found to attenuate lipid accumulation through promoting SIRT3-AMPK-mediated autophagy, mainly on lipid droplets. HK had hydrophobic interaction with amino acid residues (PHE294, GLU323 and VAL324) and NAD+. Moreover, HK improved mitochondrial function to enhance lipolysis, through decreasing the acetylated long-chain acyl-CoA dehydrogenase level. Conclusions: These results suggest that HK could ameliorate lipotoxicity in hepatocytes by activating SIRT3-AMPK-lipophagy axis, which might be a potential therapeutic agent against NAFLD.

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