Quercetin Dihydrate and Gallate Supplements Lower Plasma and Hepatic Lipids and Change Activities of Hepatic Antioxidant Enzymes in High Cholesterol-Fed Rats

2002 ◽  
Vol 72 (3) ◽  
pp. 161-169 ◽  
Author(s):  
Song-Hae Bok ◽  
Sun-Young Park ◽  
Yong Bok Park ◽  
Mi-Kyung Lee ◽  
Seon-Min Jeon ◽  
...  

This study was designed to test the lipid-lowering and antioxidant activity of two bioflavonoids, quercetin dihydrate and gallate. Four groups of rats were given a semisynthetic diet containing 10 g cholesterol/kg for six weeks. The control group received only a high-cholesterol diet, whereas the other three groups received a diet including 1 g lovastatin, 1 g quercetin dihydrate, or 1 g gallate/kg. The quercetin dihydrate and gallate supplements both significantly lowered the plasma lipid and hepatic cholesterol levels compared to those of the control. The hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity was significantly lowered by the quercetin dihydrate when compared to the other groups, while the hepatic acyl CoA:cholesterol acyltransferase (ACAT) activity was only significantly higher in the control group. The overall potential for antioxidant protection was significantly enhanced by the quercetin dihydrate and gallate supplements through lowering the plasma and hepatic thiobarbituric acid reactive substances (TBARS) levels and increasing the hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in high-cholesterol-fed rats. These results suggest that the supplementation of quercetin dihydrate and gallate promotes an increase in fecal sterols, which in turn leads to a decreased absorption of dietary cholesterol as well as lower plasma and hepatic cholesterol.

Author(s):  
Uma Narayanamurthy ◽  
Anandhi M. ◽  
Manimekalai K.

Background: Hyperlipidemia or Dyslipidemia is the major cause of atherosclerosis1 and associated conditions. Low levels of high-density-lipoprotein cholesterol (HDL-C) are the major causes of increased atherogenic risk 1. Aggressive cholesterol reduction in patients with atherosclerotic disease is now the standard of care2. In addition to life style modification, patients with risk factors need lipid lowering drug therapy. The drugs available now do not reduce LDL oxidation, and oxidative stress associated with hyperlipidemia. In recent years, antioxidants have been subjected to epidemiological studies4 that have related their consumption to a reduction in the incidence of oxidative damage related diseases.Methods: Hypercholesterolemia was induced in rats by administration of high cholesterol diet for 30 days in standard rat chow diet. Rats were divided into four groups of six each. Group-I and II with intake of normal diet and High cholesterol diet respectively. Group III and IV are given high cholesterol diet along with Lutein 50mg/kg and Atorvastatin 5mg/kg orally once daily respectively. At the end of 30 days animals were subjected to overnight fasting. Blood samples were drawn by retro-orbital puncture for biochemical analysis. The animals were sacrificed after thiopentone injection and liver and aorta were dissected out and processed for histopathological study and biochemical analysis.Results: Lutein treated group showed even more significant reduction in TBARS levels than the normal control group and Atorvastatin treated group. The efficacy of Lutein in slowing down the atherosclerosis and fatty infiltration of liver is proved in this study.Conclusions: Hence the present study had shown significant hypolipidemic, antiatherogenic and antioxidant effect of Luetin in Hyperlipidemic rats. 


Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3895-3903 ◽  
Author(s):  
Kylie N. Hewitt ◽  
Wah Chin Boon ◽  
Yoko Murata ◽  
Margaret E. E. Jones ◽  
Evan R. Simpson

Abstract The aromatase knockout (ArKO) mouse cannot synthesize endogenous estrogens due to disruption of the Cyp19 gene. We have shown previously, that ArKO mice present with age-progressive obesity and hepatic steatosis, and by 1 yr of age both male and female ArKO mice develop hypercholesterolemia. In this present study 10- to 12-wk-old ArKO mice were challenged for 90 d with high cholesterol diets. Our results show a sexually dimorphic response to estrogen deficiency in terms of cholesterol homeostasis in the liver. ArKO females presented with elevated serum cholesterol; conversely, ArKO males had elevated hepatic cholesterol levels. In response to dietary cholesterol, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase transcript levels were significantly reduced in females, whereas males showed more modest changes. Neither low density lipoprotein nor sterol regulatory element-binding protein expression levels were significantly altered by diet or genotype. The expression of Cyp7a, which encodes cholesterol 7α-hydroxylase, was significantly reduced in ArKO females compared with wild-type females and was increased by cholesterol feeding. Cyp7a expression was significantly elevated in the wild-type males on the high cholesterol diet, although no difference was seen between genotypes on the control diet. The ATP-binding cassette G5 and ATP-binding cassette G8 transporters do not appear to be regulated by estrogen. The expression of acyl-coenzyme A:cholesterol acyltransferase 2 showed a sexually dimorphic response, where estrogen appeared to have a stimulatory effect in females, but not males. This study reveals a sexually dimorphic difference in mouse hepatic cholesterol homeostasis and roles for estrogen in the regulation of cholesterol uptake, biosynthesis, and catabolism in the female, but not in the male.


2018 ◽  
Vol 10 (1) ◽  
pp. 21-26
Author(s):  
K Sharmin ◽  
R Ahmed ◽  
A Momtaz ◽  
SA Chowdhury ◽  
NA Maya ◽  
...  

Hypercholesterolemia is one of the important causes of cardiovascular disease related mortality and morbidity and recently it has become a significant issue in public health problem of developing countries. The purpose of the study was to see the effect of glycine max (soy bean) on serum lipid profile of experimentally induced hyperlipidemic rats. Hypercholesterolemia was induced by high cholesterol diet containing 1% cholesterol in olive oil. This study was done on 24 long Norwegian rats (Rattus norvegicus) weighing about 200-210 gram. For convenience, the study was divided into Experiment I and Experiment II. In experiment I, 12 rats were divided into two groups- Group A (n = 6, control group) fed on laboratory diet and Group B (n=6) fed on laboratory diet and soy bean extract for 35 days. In experiment II, the remaining 12 rats were divided into 2 groups, Group C (n=6) were fed on laboratory diet and high cholesterol diet (HCD) for 35 days and Group D (n=6) were fed laboratory diet and high cholesterol diet on initial 10 days and soy bean extract was added along with high cholesterol diet for next 25 days. Serum TC, TG, LDL-C and HDL-C were measured after 35 days. HCD increased TG, TC and LDL-C significantly in group C. Glycine max (soy bean) treated group showed that it decreased plasma TC, TG and LDL-C in experimentally induced hyperlipidemic rats but Glycine max (soy bean) did not show any significant lipid lowering effect in normolipidemic rats. The results of this experimental study indicate that Glycine max can act as a cholesterol lowering agent and thereby can improve cardiovascular functions.Bangladesh J Med Biochem 2017; 10(1): 21-26


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.


2015 ◽  
Vol 14 (34) ◽  
pp. 2604-2610
Author(s):  
M S Zamree ◽  
Safwan K Ihsan ◽  
Kamilah A K Khairul ◽  
Kamal N H Mohd ◽  
M A Rasadah ◽  
...  

2009 ◽  
Vol 37 (4) ◽  
pp. 1029-1037 ◽  
Author(s):  
Z Qiao ◽  
J Ren ◽  
H Chen

Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to atherosclerotic plaque instability and subsequent sudden coronary death. Statins are associated with decreased stroke risk and may improve stability of atherosclerotic plaques. The present study investigated the effect of simvastatin on expression of Lp-PLA2 levels in atherosclerotic plaques and on Lp-PLA2 activity in atherosclerotic aortas. Rabbits were a fed chow (control group) or a high-cholesterol diet (atherosclerosis group) for 12 weeks. An additional group on the high-cholesterol diet received simvastatin (5 mg/kg per day) for the last 4 weeks (simvastatin group). Lp-PLA2 activity in plasma and atherosclerotic aortas was significantly higher in the atherosclerosis group than in the control group and, consistent with this, abundant Lp-PLA2 protein was detected in plaques in the atherosclerosis group. Simvastatin significantly reduced Lp-PLA2 activity in plasma and aorta tissue, and reduced Lp-PLA2 protein level in atherosclerotic plaques. Whereas there was no significant difference in total atherosclerotic lesion area between simvastatin and atherosclerosis groups, simvastatin significantly reduced macrophage content, lipid retention and the intima/media ratio but increased the content of smooth muscle cells in atherosclerotic lesions. Thus, statin treatment markedly reduced Lp-PLA2 in both plasma and atherosclerotic plaques. This was associated with attenuation of the local inflammatory response and improved plaque stability.


2019 ◽  
Vol 20 (2) ◽  
pp. 76-81
Author(s):  
Jhouharotul Faradisah ◽  
Diah Purwaningsari

Dyslipidemia is an abnormal lipid metabolism which may cause fat degeneration on hepatocytes cells and elevated triglyceride serum level. Dyslipidemia can be prevented by the consumption of high antioxidant food. Noni(Morinda citrifolia) contains many antioxidant such as flavanoid, kuersetin, tannin, and saponin, which are able to prohibit the elevation of ROS.This research is aimed to find out the effect of noni(Morinda citrifolia) extract in reducing the number of hepatocyte’s cells with fat degeneration and decreasing the triglyceride level which is elevated due to high cholesterol diet induction.In this study white rats divided randomly into 4 groups, control group (K-), high cholesterol diet induced group (K+), high cholesterol diet induced with 100 mg/Kg BW noni extract group (P1), high cholesterol diet induced with 200 mg/Kg BW noni extract group (P2). The result shows that noni  extract with dose 100 mg/Kg BW and  200 mg/Kg BWcan reduce the number of hepatocytes cells with fat degeneration (p= 0,026 and p=0,027) and decrease the level of triglyceride serum (p=0,036 and p=0,010).The conclusion is noni extract with dose 100 mg/KgBW reduces effectively  the number of hepatocyte’s cells with fat degeneration and decreases the level of triglyceride serum which increase because of high cholesterol diet. 


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Swee Keong Yeap ◽  
Boon Kee Beh ◽  
Joan Kong ◽  
Wan Yong Ho ◽  
Hamidah Mohd Yusof ◽  
...  

Fermented red yeast rice has been traditionally consumed as medication in Asian cuisine. This study aimed to determine thein vivohypocholesterolemic and antioxidant effects of fermented red yeast rice water extract produced using Malaysian Agricultural Research and Development Institute (MARDI)Monascus purpureusstrains in mice fed with high cholesterol diet. Absence of monacolin-k, lower level ofγ-aminobutyric acid (GABA), higher content of total amino acids, and antioxidant activities were detected in MARDI fermented red yeast rice water extract (MFRYR).In vivoMFRYR treatment on hypercholesterolemic mice recorded similar lipid lowering effect as commercial red yeast rice extract (CRYR) as it helps to reduce the elevated serum liver enzyme and increased the antioxidant levels in liver. This effect was also associated with the upregulation of apolipoproteins-E and inhibition of Von Willebrand factor expression. In summary, MFRYR enriched in antioxidant and amino acid without monacolin-k showed similar hypocholesterolemic effect as CRYR that was rich in monacolin-k and GABA.


2018 ◽  
Vol 43 (10) ◽  
pp. 996-1002 ◽  
Author(s):  
Qi Yu ◽  
Ruihan Liu ◽  
Lijuan Han ◽  
Guangwei Zhang ◽  
Hua Guan ◽  
...  

Dietary restriction (DR) has been reported to have beneficial effects on atherosclerotic progression as well as lipid and glucose metabolism, but little is known about whether these effects can be enhanced or weakened by dietary lipid lowering. Here, after 12 weeks of high-cholesterol diet feeding, hypercholesterolemic rabbits were fed with either a standard chow diet ad libitum (AL) or a standard chow diet with DR for 16 weeks of dietary lipid lowering. We found that the DR group exhibited a loss of body weight, smaller internal organs, and reduced fat mass, while the AL group accumulated more subcutaneous fat than the baseline group. DR treatment slightly worsened glucose tolerance but enhanced insulin sensitivity, and a slight effect of DR on insulin secretion was also observed. After dietary cholesterol withdrawal, rabbits showed persistent lowering of total cholesterol and triglycerides in plasma. However, the DR group had significantly higher plasma total cholesterol than the AL group at most time points during weeks 7 to 16 of lipid lowering. Although both the AL and DR groups developed more severe atherosclerosis than the baseline group, DR did not improve atherosclerotic progression or the accumulation of macrophages and smooth muscle cells. We conclude that DR affected glucose and lipid metabolism but did not ameliorate atherosclerosis in rabbits when associated with lipid lowering by dietary cholesterol withdrawal.


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