Chlorogenic acid-enriched extract fromEucommia ulmoidesleaves inhibits hepatic lipid accumulation through regulation of cholesterol metabolism in HepG2 cells

2015 ◽  
Vol 54 (2) ◽  
pp. 251-259 ◽  
Author(s):  
Shun Hao ◽  
Yuan Xiao ◽  
Yan Lin ◽  
Zhentao Mo ◽  
Yang Chen ◽  
...  
Keyword(s):  
Chlorogenic Acid ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Cholesterol Metabolism ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Supplementation of a High-Fat Diet with Chlorogenic Acid Is Associated with Insulin Resistance and Hepatic Lipid Accumulation in Mice

2013 ◽  
Vol 61 (18) ◽  
pp. 4371-4378 ◽  
Author(s):  
Aidilla Mubarak ◽  
Jonathan M. Hodgson ◽  
Michael J. Considine ◽  
Kevin D. Croft ◽  
Vance B. Matthews
Keyword(s):  
Insulin Resistance ◽  
Chlorogenic Acid ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Dietary phosphate restriction induces hepatic lipid accumulation through dysregulation of cholesterol metabolism in mice

2013 ◽  
Vol 33 (7) ◽  
pp. 586-593 ◽  
Author(s):  
Sarasa Tanaka ◽  
Hironori Yamamoto ◽  
Otoki Nakahashi ◽  
Tomohiro Kagawa ◽  
Mariko Ishiguro ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Cholesterol Metabolism ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Dietary Phosphate

scholarly journals Apigenin Alleviates Non-Alcoholic Fatty Liver Disease by Downregulating the NLRP3/NF-κB Signaling Pathway in Mice

2021 ◽  
Author(s):  
Zheng Lu ◽  
Lu Liu ◽  
Shunxin Zhao ◽  
Jiangtao Zhao ◽  
Sujun Li
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Signaling Pathway ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation

Abstract Background: Apigenin, a flavone found in several plant foods with various biological properties including anti-inflammatory and other abilities, alleviated non-alcohol fatty liver disease (NAFLD) induced by a high fat diet (HFD) in mice. However, the mechanisms underlying this protection of inflammation and NAFLD has not been known clearly. Methods: Low density lipoprotein receptor-deficient (Ldlr-/-) mice were fed with HFD diet to induce NAFLD model and were treated with apigenin (50 mg/kg/day) for eight weeks. Hepatic lipid accumulation and inflammation in the livers were analyzed and quantified. In vitro experiments, HepG2 cells were stimulated by LPS plus oleic acid (OA) in the absence of presence of apigenin (50μM). Lipid accumulation and the effect of apigenin on NLRP3/NF-κB signaling pathway was investigated.Results: Apigenin administration reduce the weight, plasma lipid levels in Ldlr-/- mice when fed an HFD. Apigenin (50 mg/kg/day) treated mice displayed reduced hepatic lipid accumulation and inflammation in the livers of mice given the HFD diet. Treating the HepG2 cells with apigenin reduced lipid accumulation. And, apigenin also inhibited activation of NLRP3/NF-κB signaling pathway stimulated by OA together with LPS. Conclusions: Our results indicated that apigenin supplementation prevented NAFLD via down-regulating the NLRP3/NF-κB signaling pathway in mice, and suggested apigenin might be a potential therapeutic agent for the prevention of NAFLD.

Corosolic Acid Attenuates Hepatic Lipid Accumulation and Inflammatory Response via AMPK/SREBPs and NF-κB/MAPK Signaling Pathways

2020 ◽  
Vol 48 (03) ◽  
pp. 579-595
Author(s):  
Jian-Xiu Zhang ◽  
Wei-Jun Feng ◽  
Guan-Cheng Liu ◽  
Qian-Qian Ma ◽  
Hai-Lan Li ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Lipid Accumulation ◽  
Hepg2 Cells ◽  
Density Lipoprotein ◽  
Mapk Signaling ◽  
Lipoprotein Cholesterol ◽  
Hepatic Lipid ◽  
Hepatic Lipid Accumulation ◽  
Corosolic Acid ◽  
Mapk Signaling Pathways

Corosolic acid (CA) is the main active component of Lagetstroemia speciosa and has been known to serve as several different pharmacological effects, such as antidiabetic, anti-oxidant, and anticancer effects. In this study, effects of CA on the hepatic lipid accumulation were examined using HepG2 cells and tyloxapol (TY)-induced hyperlipidemia ICR mice. CA significantly inhibited hepatic lipid accumulation via inhibition of SREBPs, and its target genes FAS, SCD1, and HMGCR transcription in HepG2 cells. These effects were mediated through activation of AMPK, and these effects were all abolished in the presence of compound C (CC, an AMPK inhibitor). In addition, CA clearly alleviated serum ALT, AST, TG, TC, low-density lipoprotein cholesterol (LDL-C), and increased high-density lipoprotein cholesterol (HDL-C) levels, and obviously attenuated TY-induced liver steatosis and inflammation. Moreover, CA significantly upregulated AMPK, ACC, LKB1 phosphorylation, and significantly inhibited lipin1, SREBPs, TNF-[Formula: see text], F4/80, caspase-1 expression, NF-[Formula: see text]B translocation, and MAPK activation in TY-induced hyperlipidemia mice. Our results suggest that CA is a potent antihyperlipidemia and antihepatic steatosis agent and the mechanism involved both lipogenesis and cholesterol synthesis and inflammation response inhibition via AMPK/SREBPs and NF-[Formula: see text]B/MAPK signaling pathways.

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