scholarly journals Glucose induced hepatic lipase expression and ApoB100/ApoAI ratio changes in cultured HepG2 cells in vitro

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 842
Author(s):  
Minshan Hu
Keyword(s):  
Coronary Artery Disease ◽  
Hepg2 Cells ◽  
Hepatic Lipase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Regulatory Pathway ◽  
Hepatic Lipase Activity ◽  
Artery Disease ◽  
Lipase Expression ◽  
Novel Therapeutic

Backgroundː Hepatic lipase (HL) plays a very important role in lipoprotein catabolism. The aim of this study was to measure both HL activity and ApoB100/ApoAI ratio changes in cell secretions by incubating HepG2 cells with various amounts of glucose. Methodsː HepG2 cells were cultured in low-, normal- or high-glucose Dulbecco's Modified Eagle Medium (DMEM) (1, 4.5 and 10g/L, respectively). HL activities were determined using the Hepatic Lipase Detection Kit (cat. no. A067) from Nanjing Jiancheng Bioengineering Institute (Nanjing, China). Levels of ApoAI and ApoB100 were measured with commercial sandwich enzyme-linked immunosorbent assay kits (cat#: H0123 and H0124) from ShangHai MEIXUAN Biological Science and Technology Ltd (Shanghai, China). Experiments were repeated six times for each assay. Resultsː Pearson’s correlation coefficient results showed that ApoB100 and ApoB100/ApoAI ratio have positive and significant correlations with HL activity, and ApoAI has a negative and significant correlation with HL activity. Conclusionsː Glucose may increase or decrease ApoB100/ApoAI ratio through upregulation or downregulation of hepatic lipase activity, which suggests a new regulatory pathway in lipoprotein catabolism. This finding may lead to novel therapeutic ways for diagnosis and treatment for coronary artery disease.

Low hepatic lipase activity is a risk factor for coronary artery disease

2000 ◽  
Vol 151 (1) ◽  
pp. 126 ◽  
Author(s):  
K.A. Dugi ◽  
K. Brandauer ◽  
N. Schmidt ◽  
D. Ramacher ◽  
J. Kreuzer
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Lipase Activity ◽  
Hepatic Lipase ◽  
Hepatic Lipase Activity ◽  
Artery Disease

scholarly journals Glucose induced ApoB100/ApoAI ratio changes in cultured HepG2 cells in vitro

F1000Research ◽  
2022 ◽  
Vol 10 ◽  
pp. 842
Author(s):  
Minshan Hu
Keyword(s):  
Hepg2 Cells ◽  
Cell Model ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mechanism Study ◽  
A Cell ◽  
Ratio Change ◽  
Artery Disease ◽  
Positive Correlations

Backgroundː Numerous in vivo human cohort studies have suggested that the apolipoprotein B100/apolipoprotein AI (ApoB100/ApoAI) ratio might be a risk factor in coronary heart disease. The aim of this study was to measure ApoB100/ApoAI ratio changes in cell secretions by incubating HepG2 cells with various amounts of glucose in vitro. Methods ː HepG2 cells were cultured in low-, normal- or high-glucose Dulbecco's Modified Eagle Medium (DMEM) (1, 4.5 and 10g/L, respectively). Levels of ApoAI and ApoB100 were measured with commercial sandwich enzyme-linked immunosorbent assay kits (cat#: H0123 and H0124) from ShangHai MEIXUAN Biological Science and Technology Ltd (Shanghai, China). Experiments were repeated six times for each assay. Resultsː The results showed that ApoB100/ApoAI ratio have positive correlations with the glucose concentration increase. Conclusionsː A higher concentration of glucose induced an undesirable ApoB100/ApoAI ratio change, which suggests a new regulatory pathway in lipoprotein catabolism and provides a cell model for further mechanism study. This finding may lead to novel therapeutic ways for diagnosis and treatment for coronary artery disease.

scholarly journals LDL triglycerides, hepatic lipase activity, and coronary artery disease: An epidemiologic and Mendelian randomization study

2019 ◽  
Vol 282 ◽  
pp. 37-44 ◽  
Author(s):  
Günther Silbernagel ◽  
Hubert Scharnagl ◽  
Marcus E. Kleber ◽  
Graciela Delgado ◽  
Tatjana Stojakovic ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Lipase Activity ◽  
Mendelian Randomization ◽  
Hepatic Lipase ◽  
Hepatic Lipase Activity ◽  
Artery Disease

scholarly journals Low Hepatic Lipase Activity Is a Novel Risk Factor for Coronary Artery Disease

Circulation ◽  
2001 ◽  
Vol 104 (25) ◽  
pp. 3057-3062 ◽  
Author(s):  
Klaus A. Dugi ◽  
Karin Brandauer ◽  
Nikolaus Schmidt ◽  
Barbara Nau ◽  
Jochen G. Schneider ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Lipase Activity ◽  
Hepatic Lipase ◽  
Hepatic Lipase Activity ◽  
Artery Disease

Das Komplementsystem

2012 ◽  
Vol 32 (04) ◽  
pp. 276-285 ◽  
Author(s):  
V. Frauenknecht ◽  
V. Schroeder
Keyword(s):  
Coronary Artery Disease ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
The Other ◽  
Atherosclerotic Plaques ◽  
Inflammatory Processes ◽  
Artery Disease ◽  
The Complement System ◽  
Novel Therapeutic

SummaryAtherosclerotic diseases such as coronary artery disease and ischaemic stroke are caused by chronic inflammation in arterial vessel walls. The complement system is part of the innate immune system. It is involved in many processes contributing to onset and development of atherosclerotic plaques up to the final stage of acute thrombotic events. This is due to its prominent role in inflammatory processes. In addition, there is increasing evidence that interactions between complement and coagulation provide a link between inflammation and thrombosis. On the other hand, the complement system also has an atheroprotective function through the clearance of apoptotic material.The knowledge of these complex mechanisms will become increasingly important, also for clinicians, since it may lead to novel therapeutic and diagnostic options. Therapies targeting the complement system have the potential to reduce tissue damage caused by acute ischaemic events. Whether early anti-inflammatory and anti-complement therapy may be able to prevent atherosclerosis, remains a hot topic for research.

Monocyte-derived dendritic cells of patients with coronary artery disease show an increased expression of costimulatory molecules CD40, CD80 and CD86 in vitro

2007 ◽  
Vol 18 (7) ◽  
pp. 523-531 ◽  
Author(s):  
Jörn F. Dopheide ◽  
Urban Sester ◽  
Axel Schlitt ◽  
Georg Horstick ◽  
Hans J. Rupprecht ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Dendritic Cells ◽  
Coronary Artery ◽  
Costimulatory Molecules ◽  
Artery Disease

In Vitro Simultaneous Transfer of Lipids to HDL in Coronary Artery Disease and in Statin Treatment

Lipids ◽  
2009 ◽  
Vol 44 (10) ◽  
pp. 917-924 ◽  
Author(s):  
Ana C. Lo Prete ◽  
Clederson H. Dina ◽  
Carolina H. Azevedo ◽  
Camila G. Puk ◽  
Neuza H. M. Lopes ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Statin Treatment ◽  
Simultaneous Transfer ◽  
Artery Disease

scholarly journals IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

2021 ◽  
Author(s):  
Mina Mohammad-Rezaei ◽  
Reza Ahmadi ◽  
Ali Rafiei ◽  
Arsalan Khaledifar ◽  
Shohila Fatahi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Levels ◽  
Arterial Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Tnf Α ◽  
Significant Difference ◽  
Major Vessel ◽  
Artery Disease

Abstract Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

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