Paraoxonase-1 Deficiency Is Associated with Severe Liver Steatosis in Mice Fed a High-fat High-cholesterol Diet: A Metabolomic Approach

2013 ◽  
Vol 12 (4) ◽  
pp. 1946-1955 ◽  
Author(s):  
Anabel García-Heredia ◽  
Elizabeth Kensicki ◽  
Robert P. Mohney ◽  
Anna Rull ◽  
Iris Triguero ◽  
...  
Keyword(s):  
Liver Steatosis ◽  
Paraoxonase 1 ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Severe Liver ◽  
Metabolomic Approach

scholarly journals CBD Alleviates Liver Injuries in Alcoholics With High-Fat High-Cholesterol Diet Through Regulating NLRP3 Inflammasome–Pyroptosis Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Xuye Jiang ◽  
Yingying Gu ◽  
Yuanling Huang ◽  
Yujia Zhou ◽  
Nengzhi Pang ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Nlrp3 Inflammasome ◽  
Liver Diseases ◽  
Liver Steatosis ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Alcoholic Fatty Liver ◽  
Liver Injuries

Alcohol abuse and high-fat diet–induced liver diseases have been the most prevalent chronic liver diseases and the leading reasons for liver transplantation around the world. Cannabidiol (CBD) is a botanical component extracted from marijuana plants without psychoactive impact. In our previous reports, we found that CBD can prevent fatty liver induced by Lieber–DeCarli ethanol diet or non-alcoholic fatty liver disease (NAFLD) induced by high-fat high-cholesterol diet. The current work is a further study on whether CBD can alleviate liver injuries induced by ethanol plus high-fat high-cholesterol diet (EHFD), which is a model simulating heavy alcohol drinkers in a Western diet. A mice liver injury model induced by EHFD for 8 weeks was applied to explore the protective properties of CBD and the underlying mechanisms. We found that CBD prevented liver steatosis and oxidative stress induced by EHFD. CBD treatment inhibited macrophage recruitment and suppressed activation of NFκB–NLRP3–pyroptosis pathway in mice livers. The hepatoprotective property of CBD in the current model might be a result of inhibition of inflammation via alleviating activation of the hepatic NFκB–NLRP3 inflammasome–pyroptosis pathway by CBD.

Sub-chronic microcystin-LR renal toxicity in rats fed a high fat/high cholesterol diet

Chemosphere ◽  
2020 ◽  
pp. 128773
Author(s):  
Tarana Arman ◽  
Katherine D. Lynch ◽  
Michael Goedken ◽  
John D. Clarke
Keyword(s):  
Renal Toxicity ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

scholarly journals Interleukin-18 predicts atherosclerosis progression in SIV-infected and uninfected rhesus monkeys (Macaca mulatta) on a high-fat/high-cholesterol diet

2009 ◽  
Vol 89 (6) ◽  
pp. 657-667 ◽  
Author(s):  
Jennifer H Yearley ◽  
Dongling Xia ◽  
Christine B Pearson ◽  
Angela Carville ◽  
Richard P Shannon ◽  
...  
Keyword(s):  
Macaca Mulatta ◽  
Rhesus Monkeys ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
Interleukin 18 ◽  
High Cholesterol ◽  
High Fat ◽  
Atherosclerosis Progression

Abstract 130: Hypercholesterolemia Suppresses Carotid Artery Endothelial NOS3 Expression via Epigenetic Mechanisms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Alex Sotolongo ◽  
Yi-Zhou Jiang ◽  
John Karanian ◽  
William Pritchard ◽  
Peter Davies
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Endothelial Cells ◽  
Dna Methyltransferase ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat

Objective: One of the first clinically detectable changes in the vasculature during atherogenesis is the accumulation of cholesterol within the vessel wall. Hypercholesterolemia is characterized by dysfunctional endothelial-dependent vessel relaxation and impaired NOS3 function. Since DNA methylation at gene promoter regions strongly suppresses gene expression, we postulated that high-fat/high-cholesterol diet suppresses endothelial NOS3 through promoter DNA methylation. Methods: Domestic male pigs were fed control diet (CD) or isocaloric high fat and high cholesterol diet (HC; 12% fat and 1.5% cholesterol) for 2, 4, 8 or 12 weeks prior to tissue collection. Furthermore, to determine the effects of risk factor withdrawal, an additional group of swine received HC for 12 weeks and then CD for 8 weeks; a control group received HC continuously for 20 weeks. Endothelial cells were harvested from common carotid aorta. In parallel in vitro studies, cultured human aortic endothelial cells (HAEC) were treated with human LDL, GW3956 (LXR agonist) and RG108 (DNA methyltransferase [DNMT] inhibitor). In cells from both sources, DNA methylation at the NOS3 promoter was measured using methylation specific pyro sequencing, and endothelial gene expression was measured using RT PCR. Results: HC diet increased plasma cholesterol level from 75 mg/dl on CD to a plateau of about 540 mg/dl within 2 weeks. Endothelial NOS3 expression was significantly reduced (71±9 % of CD) after 4 weeks of HC, a level sustained at subsequent time points. Withdrawal of HC for 8 weeks did not recover NOS3 expression. After 12-week HC, the NOS3 promoter was hypermethylated. Withdrawal of HC did not reverse NOS3 promoter methylation. In vitro treatment of HAEC with human LDL (200 mg/dl total cholesterol) or GW3956 (5μM) suppressed NOS3 mRNA to 50% and 30% respectively, suggesting that LXR/RXR is involved in suppression of NOS3. Nitric oxide production was consistently suppressed by GW3959. Both could be reversed through inhibition of DNMTs by RG108. Conclusions: DNA methylation and LXR/RXR pathway can mediate the HC-suppression of endothelial NOS3. The study identifies novel pharmaceutical targets in treating endothelial dysfunction. Crosstalk between these pathways is under investigation.

scholarly journals Mangosteen Pericarp Inhibits Nuclear Factor ?B (NF-?B) Activation and Reduces Expression of ICAM-1 in High Cholesterol Diet Rat

2013 ◽  
pp. 23-32
Author(s):  
H Hendarto ◽  
Mohammad Saifur Rohman ◽  
Djanggan Sargowo
Keyword(s):  
Crude Extract ◽  
High Fat Diet ◽  
Inhibitory Effect ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
High Fat ◽  
Factor B ◽  
Underlying Risk Factor ◽  
Underlying Risk

Background: Atherosclerosis is widely viewed as an inflammatory disease with hypercholesterolemia being a dominant underlying risk factor. This study aimed to determine the effect of mangosteen pericarp in inhibition of NF-?B activation and ICAM-1 expression in rat fed with high cholesterol.Methods and Results: Various doses of crude extract mangosteen pericarp were administered to the high fat diet wistar rats and the activity of NF-?B measured by immunohistochemistry to assess nuclear NF-?B expression and the ICAM-1 expression. The high fat diet resulted significant increased serum LDL levels. Increased nuclear NF- ?B activation and ICAM-1 expression were also observed in high fat diet rats in concurrence with increased serum LDL. The inhibitory effect on NF- ?B activity and ICAM-1 expression was observed when 400 mg of mangosteen pericarp crude extract was administered and even showed a higher inhibitory effect in 800 mg of mangosteen pericap treated rats. The 800 mg extract treatment resulted in decreased ICAM-1 expression similar to those of non high fat rats.Conclusion: The administration of 800 mg mangosteen pericarp crude extract significantly inhibited NF-?B activation and reversed the expression of ICAM -1 to the normal level in high cholesterol diet rats.

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