W01.88 Reduction of plasma oxidized LDL concentration but not change of LDL oxidation level following treatment of familial hypercholesterolemia patients with statins

2004 ◽  
Vol 5 (1) ◽  
pp. 20
Author(s):  
L VANTITS
Keyword(s):  
Familial Hypercholesterolemia ◽  
Oxidized Ldl ◽  
Ldl Oxidation ◽  
Oxidation Level

scholarly journals Anti-Atherosclerotic Activity of (3R)-5-Hydroxymellein from an Endophytic Fungus Neofusicoccum parvum JS-0968 Derived from Vitex rotundifolia through the Inhibition of Lipoproteins Oxidation and Foam Cell Formation

Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 715
Author(s):  
Jae-Yong Kim ◽  
Soonok Kim ◽  
Sang Hee Shim
Keyword(s):  
Conformational Changes ◽  
Endophytic Fungus ◽  
Foam Cell ◽  
Oxidized Ldl ◽  
Cell Formation ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Foam Cell Formation ◽  
Macrophage Foam Cell ◽  
Neofusicoccum Parvum

An endophytic fungus, Neofusicoccum parvum JS-0968, was isolated from a plant, Vitex rotundifolia. The chemical investigation of its cultures led to the isolation of a secondary metabolite, (3R)-5-hydroxymellein. It has been reported to have antifungal, antibacterial, and antioxidant activity, but there have been no previous reports on the effects of (3R)-5-hydroxymellein on atherosclerosis. The oxidation of lipoproteins and foam cell formation have been known to be significant in the development of atherosclerosis. Therefore, we investigated the inhibitory effects of (3R)-5-hydroxymellein on atherosclerosis through low-density lipoprotein (LDL) and high-density lipoprotein (HDL) oxidation and macrophage foam cell formation. LDL and HDL oxidation were determined by measuring the production of conjugated dienes and malondialdehyde, the amount of hyperchromicity and carbonyl content, conformational changes, and anti-LDL oxidation. In addition, the inhibition of foam cell formation was measured by Oil red O staining. As a result, (3R)-5-hydroxymellein suppressed the oxidation of LDL and HDL through the inhibition of lipid peroxidation, the decrease of negative charges, the reduction of hyperchromicity and carbonyl contents, and the prevention of apolipoprotein A-I (ApoA-I) aggregation and apoB-100 fragmentation. Furthermore, (3R)-5-hydroxymellein significantly reduced foam cell formation induced by oxidized LDL (oxLDL). Taken together, our data show that (3R)-5-hydroxymellein could be a potential preventive agent for atherosclerosis via obvious anti-LDL and HDL oxidation and the inhibition of foam cell formation.

Differences in phenotype, genotype and cardiovascular events between patients with probable and definite heterozygous familial hypercholesterolemia

2019 ◽  
Vol 16 (6) ◽  
pp. 467-478
Author(s):  
Ye-Xuan Cao ◽  
Bing-Yang Zhou ◽  
Di Sun ◽  
Sha Li ◽  
Yuan-Lin Guo ◽  
...  
Keyword(s):  
Familial Hypercholesterolemia ◽  
Cardiovascular Events ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Survival Rates ◽  
Gene Mutations ◽  
Density Lipoprotein ◽  
Heterozygous Familial Hypercholesterolemia ◽  
Lipid Clinic ◽  
Kaplan Meier

Aim: To investigated the potential differences between probable and definite heterozygous familial hypercholesterolemia (HeFH) patients diagnosed by Dutch Lipid Clinic Network criteria. Methods: Clinical characteristics, lipid profile, severity of coronary artery stenosis and gene mutations were compared. Kaplan–Meier curve was performed to evaluate the cardiovascular events. Results: Overall, 325 participants were included and divided into two groups: probable (n = 233) and definite HeFH (n = 92). Definite HeFH patients had higher low-density lipoprotein cholesterol (LDL-C), oxidized-LDL and proprotein convertase subtilisin/kexin 9 levels, and higher prevalence of tendon xanthomas. The incidence of genetic mutations was statistically higher in definite HeFH than probable HeFH patients. The coronary stenosis calculated by Gensini score was statistically severer in definite HeFH patients. The best LDL-C threshold for predicting mutations was 5.14 mmol/l. Definite HeFH had lower event-free survival rates. Conclusion: Definite HeFH patients had higher severity of phenotype and genotype, and higher risk of cardiovascular events.

scholarly journals New pathogenetic hypothesis for Wolman disease: possible role of oxidized low-density lipoproteins in adrenal necrosis and calcification

1994 ◽  
Vol 301 (1) ◽  
pp. 267-273 ◽  
Author(s):  
G Fitoussi ◽  
A Nègre-Salvayre ◽  
M T Pieraggi ◽  
R Salvayre
Keyword(s):  
Cytotoxic Effect ◽  
Oxidized Ldl ◽  
Low Density Lipoproteins ◽  
Ldl Oxidation ◽  
Low Density ◽  
Cholesteryl Esters ◽  
Lysosomal Degradation ◽  
Wolman Disease ◽  
Adrenal Cells ◽  
Oxidized Low Density Lipoproteins

Wolman disease in an inherited metabolic disease, characterized by a severe deficiency of the acid lipase and a massive lysosomal storage of triacylglycerols and cholesteryl esters, associated with hepatosplenomegaly, adrenal calcification and nearly always fatal in the first year of life. Cultured human lymphoblastoid cells and human adrenal cells are able to promote the formation of mildly oxidized low-density lipoproteins (LDL), which in turn exhibit a non-negligible cytotoxic effect on these cells. In contrast, fibroblasts induce only very low levels of LDL oxidation. Comparative experiments have shown that the cytotoxic effect of oxidized LDL was higher to Wolman-disease cells than to controls. The oxidative ability of Wolman cells was similar to that of normal ones. The over-cytotoxicity of mildly oxidized LDL to Wolman cells resulted from the higher uptake of mildly oxidized LDL through the LDL-receptor pathway, which is only poorly down-regulated in Wolman cells subsequently to the block of the lysosomal degradation of LDL-cholesteryl esters. In cultured adrenal cells, oxidized LDL induced a sustained rise in intracellular [Ca2+] which is directly involved in the cellular damage and cell death induced by oxidized LDL [Nègre-Salvayre and Salvayre (1992) Biochim. Biophys. Acta 1123, 207-215]. This Ca2+ peak is followed by a dramatic deposition of calcium in damaged or/and dead cultured adrenal cells, quite similar to that observed in Wolman-disease adrenal cortex. The cell-induced LDL oxidation and the subsequent cytotoxic effect can be prevented, at least in part, by antioxidants such as alpha-tocopherol and nordihydroguaiaretic acid. These findings support the hypothesis that the Wolman-disease adrenal damage (necrosis and calcification) could result from the association of the following events: mild oxidation of LDL by adrenal cells, over-uptake of mildly oxidized LDL by Wolman cells (resulting from the block of the lysosomal degradation of cholesteryl esters in Wolman cells), and cytotoxicity related to the amount of mildly oxidized LDL internalized by cells. The reported data also suggest that LDL oxidation induced by adrenal cells and their subsequent cytotoxicity can be prevented (in part) by antioxidants, and the potential therapeutic use of antioxidants in Wolman disease is discussed.

Protective Effects of Berberine against Low-Density Lipoprotein (LDL) Oxidation and Oxidized LDL-Induced Cytotoxicity on Endothelial Cells

2007 ◽  
Vol 55 (25) ◽  
pp. 10437-10445 ◽  
Author(s):  
Yih-Shou Hsieh ◽  
Wu-Hsien Kuo ◽  
Ta-Wei Lin ◽  
Horng-Rong Chang ◽  
Teseng-His Lin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Ldl Oxidation ◽  
Low Density ◽  
Protective Effects

scholarly journals EFFECTIVENESS OF LEAF EXTRACT REDUCE INFLAMMATION REACTION IN HYPERCHOLESTEROLEMIA RATS

2017 ◽  
Vol 1 (1) ◽  
pp. 12
Author(s):  
Puguh Santoso ◽  
Ni Nyoman Wahyu Udayani ◽  
I Nyoman Gede Tri Sutrisna ◽  
Ketut Agus Adrianta
Keyword(s):  
Free Radicals ◽  
Leaf Extract ◽  
Oxidized Ldl ◽  
Oxidative Modification ◽  
Blood Cholesterol ◽  
Ldl Oxidation ◽  
Control Group ◽  
Control Group Design ◽  
White Rats ◽  
Group I

Abstract High blood cholesterol is often called hypercholesterolemia is a risk factor for the emergence of pathological conditions such as heart and blood vessel disease. Hypercholesterolemia has an important role in the occurrence of damage to the endothelial cells is mainly caused by oxidized LDL. Oxidation of LDL triggers the formation of TNF - ?. Leaves messengers that allegedly contains flavonoids can improve the situation of hypercholesterolemia through the barriers specifically the expression of TNF - ? increased due to hypercholesterolemia. Plants messengers known to contain alkaloids, flavonoids, tannins, saponins, polyphenols, calcium oxalate, fats, and essential oil. Flavonoids which has the ability to bind the atom to form free radicals not to excess free radicals, thereby inhibiting the oxidative modification of LDL become ox-LDL so it will not be formed atherosclerosis. This study uses the Randomize pattern Pre and Post Test Control Group Design, using white rats (Rattusnovergicus) with Wistar strain aged 3-4 months, weighing 175-200 grams. Divided into four groups: Group I as a control with placebo, Group II treatment using extracts of ethanol leaves a messenger at a concentration of 10%, Group III treatments using extracts of ethanol leaves a messenger at a concentration of 20%, Group IV is to use the extract ethanol leaves errand at a concentration of 30%. It can be concluded at 4 dose group 30% messengers leaf extract significantly different, p <0.05, so it can be said that the provision of effective messengers extract at a dose of 30%.

Lipid and lipoprotein profile in women with polycystic ovary syndromeThis article is one of a selection of papers published in the special issue Bridging the Gap: Where Progress in Cardiovascular and Neurophysiologic Research Meet.

2008 ◽  
Vol 86 (4) ◽  
pp. 199-204 ◽  
Author(s):  
Djuro Macut ◽  
Dimitrios Panidis ◽  
Biljana Glišić ◽  
Nikolaos Spanos ◽  
Milan Petakov ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Polycystic Ovary ◽  
Oxidized Ldl ◽  
Sex Hormone Binding Globulin ◽  
Ldl Oxidation ◽  
Model Assessment ◽  
Homa Index ◽  
Nonesterified Fatty Acids ◽  
Increased Risk

Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by obesity-related risk factors for cardiovascular disease. The objective of our study was to determine values of key lipid and lipoprotein fractions in PCOS, and their possible relation to insulin resistance. A total of 75 women with PCOS (aged 23.1 ± 5.1 years, BMI 24.9 ± 4.7 kg/m2), and 56 age- and BMI-matched controls were investigated. In all subjects, basal glucose, cholesterol (total, HDL, and LDL), oxidized LDL (OxLDL), triglycerides, apolipoprotein (apo)A1, apoB, and apoE, nonesterified fatty acids, insulin, testosterone, sex hormone-binding globulin, homeostasis model assessment (HOMA) index, and free androgen index were determined in the follicular phase of the cycle. PCOS patients compared with controls had increased indices of insulin resistance, basal insulin (p < 0.001), and HOMA index (p < 0.001), and worsened insulin resistance-related dyslipidemia with decreased HDL cholesterol (p < 0.01), elevated triglycerides (p = 0.010), and pronounced LDL oxidation (p < 0.001). In conclusion, characteristic dyslipidemia of insulin resistance and unfavorable proatherogenic lipoprotein ratios were present only in women with PCOS and not in controls. Elevated OxLDL and the relation of apoE and nonesterified fatty acids with insulin resistance suggest that women with PCOS are at increased risk for premature atherosclerosis.

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