Lipid-Lowering Effect of Eriocitrin, the Main Flavonoid in Lemon Fruit, in Rats on a High-Fat and High-Cholesterol Diet

2006 ◽  
Vol 71 (9) ◽  
pp. S633-S637 ◽  
Author(s):  
Yoshiaki Miyake ◽  
Eriko Suzuki ◽  
Satoko Ohya ◽  
Syuichi Fukumoto ◽  
Masanori Hiramitsu ◽  
...  
2009 ◽  
Vol 46 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Thamolwan Suanarunsawat ◽  
Watcharaporn Devakul Na Ayutthaya ◽  
Thanapat Songsak ◽  
Suwan Thirawarapan ◽  
Somlak Poungshompoo

2012 ◽  
Vol 90 (9) ◽  
pp. 1185-1196 ◽  
Author(s):  
Verónica D’Annunzio ◽  
Martín Donato ◽  
Bruno Buchholz ◽  
Virginia Pérez ◽  
Verónica Miksztowicz ◽  
...  

Ischemic heart disease is the leading cause of morbi-mortality in developed countries. Both ischemia–reperfusion injury and mechanisms of cardioprotection have been studied for more than 50 years. It is known that the physiopathological mechanism of myocardial ischemia involves several factors that are closely related to its development, of which hypercholesterolemia is one of the main ones. Therefore, the objective of this review was to elucidate the effects of a high-cholesterol diet on normal ventricular function and ischemia–reperfusion injury associated phenomenon such as post-ischemic ventricular dysfunction (stunned myocardium). Although there exist many studies considering several aspects of this physiopathological entity, the majority were carried out on normal animals. Thus, experiments carried out on hypercholesterolemic models are controversial, in particular those evaluating different mechanisms of cardioprotection such as ischemic preconditioning and postconditioning, and cardioprotection granted by drugs such as statins, which apart from exerting a lipid-lowering effect, exert pleiotropic effects providing cardioprotection against ischemia–reperfusion injury. These controversial results concerning the mechanisms of cardioprotection vary according to quality, composition, and time of administration of the high-cholesterol diet, as well as the species used in each experiment. Thus, to compare the results it is necessary to take all of these variables into account, since they can change the obtained results.


2019 ◽  
Vol 31 (1) ◽  
pp. 52-61
Author(s):  
Sagia Afrose ◽  
Md Ismail Khan ◽  
Elisa Omar Eva ◽  
Mohammad Imtiaj Mahbub

Background: Hypercholesterolemia is a condition characterized by very high level of cholesterol in the blood. Too much cholesterol increases risk of developing heart disease called coronary artery disease. This condition occurs when excess cholesterol in the bloodstream is deposited in the walls of blood vessels, particularly in the coronary arteries that supply blood to the heart. A phenolic compound of the cinnamon extract lowers serum lipid level by inhibiting HMG COA reductase & by activation of nuclear receptor peroxisome proliferator activated receptor alpha (PPAR-α). We are trying to evaluate the lipid lowering effect of cinnamon (Cinnamomum cassiae) in comparison with rosuvastatin in hypercholesterolaemic rats. Aim: To find out the lipid lowering effect of aqueous extract of cinnamon (Cinnamomum cassiae) and compare it with a established lipid lowering drug (rosuvastatin) on hypercholesterolaemic rats. Method: This was a experimental study conducted in the department of Pharmacology, Dhaka medical college & Hospital from July 2015 to June 2016. Sample size was 30.The study was designed as 2 parts: Experiment-1 & Experiment -2. Result: Cinnamon produces no statistically significant effect on serum lipid level of healthy rats (P- value >0.05; which is not significant). Cinnamon significantly reduced serum lipid level of high cholesterol diet induced hypercholesterolaemic rats. But, there is statistically significant difference between cinnamon and rosuvastatin lipid lowering effect in high cholesterol diet induced hypercholesterolaemic rats (p value <0.05; which is significant). Conclusion: The study was conducted to find out lipid lowering effect of cinnamon on experimentally induced hypercholesterolaemic rats. The present study found that cinnamon (Cinnamomum cassaiae) significantly lowers serum lipid level in experimentally induced hypercholesterolaemic rats. So cinnamon can be used as alternative lipid lowering agent for its easy availability, cost effectiveness and as well as lack of significant side effects. TAJ 2018; 31(1): 52-61


2009 ◽  
Vol 53 (6) ◽  
pp. 751-759 ◽  
Author(s):  
Myung-Sook Choi ◽  
Mi-Kyung Lee ◽  
Un Ju Jung ◽  
Hye-Jin Kim ◽  
Geoyng-Min Do ◽  
...  

Chemosphere ◽  
2020 ◽  
pp. 128773
Author(s):  
Tarana Arman ◽  
Katherine D. Lynch ◽  
Michael Goedken ◽  
John D. Clarke

2009 ◽  
Vol 89 (6) ◽  
pp. 657-667 ◽  
Author(s):  
Jennifer H Yearley ◽  
Dongling Xia ◽  
Christine B Pearson ◽  
Angela Carville ◽  
Richard P Shannon ◽  
...  

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Alex Sotolongo ◽  
Yi-Zhou Jiang ◽  
John Karanian ◽  
William Pritchard ◽  
Peter Davies

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.


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