Journal articles: 'Hypercholesterolemie'

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Nussbaumerová, Barbora, and Hana Rosolová. "Epidemiology of hypercholesterolemia." Vnitřní lékařství 64, no. 1 (January 1, 2018): 30–37. http://dx.doi.org/10.36290/vnl.2018.005.

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DE BACKER G. "Geïsoleerde hypercholesterolemie." Tijdschrift voor Geneeskunde 55, no. 22 (January 1, 1999): 1625. http://dx.doi.org/10.2143/tvg.55.22.5000602.

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DE BACKER G. "Geïsoleerde hypercholesterolemie." Tijdschrift voor Geneeskunde, no. 22 (January 1, 1999): 1625. http://dx.doi.org/10.47671/tvg.55.22.5000602.

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Češka, Richard, Michaela Šnejdrlová, Michal Vrablík, Tereza Altschmiedová, and Tomáš Štulc. "Treating hypercholesterolaemia with evolocumab." Intervenční a akutní kardiologie 17, no. 4 (December 1, 2018): 212–17. http://dx.doi.org/10.36290/kar.2018.057.

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VAN CLEEMPUT J. "Zware hypercholesterolemie: behandeling?" Tijdschrift voor Geneeskunde, no. 4 (2009): 159–60. http://dx.doi.org/10.47671/tvg.65.04.2000488.

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Karásek, David. "Ezetimibe in the treatment of hypercholesterolaemia." Interní medicína pro praxi 21, no. 2 (May 10, 2019): 112–16. http://dx.doi.org/10.36290/int.2019.017.

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. "Therapietrouw bij familiaire hypercholesterolemie." Medisch-Farmaceutische Mededelingen 41, no. 6 (June 2003): 180. http://dx.doi.org/10.1007/bf03058199.

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Broekhuizen, Lidewij. "Spoor familiaire hypercholesterolemie op." Huisarts en wetenschap 60, no. 1 (January 2017): 3. http://dx.doi.org/10.1007/s12445-017-0003-1.

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Lafeber, M., and GA Rongen. "PCSK9-remmers bij familiaire hypercholesterolemie." Ge-Bu 108-115, no. 10 (2021): 1. http://dx.doi.org/10.35351/gebu.nl.2021.10.20.

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Wiegman, A. "Vetstofwisselingsafwijkingen bij kinderenfamiliaire hypercholesterolemie cholesterol." Bijblijven 19, no. 2 (February 2003): 79–82. http://dx.doi.org/10.1007/bf03059691.

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Soška, Vladimír, and Ondřej Kyselák. "New options in the treatment of hypercholesterolaemia." Interní medicína pro praxi 18, no. 1 (February 1, 2016): 6–8. http://dx.doi.org/10.36290/int.2016.002.

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. "Knoflook in de behandeling van hypercholesterolemie." Medisch-Farmaceutische Mededelingen 39, no. 11 (November 2001): 243. http://dx.doi.org/10.1007/bf03057806.

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Urbánek, Robin, Lukáš Tichý, and Tomáš Freiberger. "Tangier disease in family with the phenotype of familial hypercholesterolemia." Vnitřní lékařství 66, no. 7 (November 3, 2020): 443–46. http://dx.doi.org/10.36290/vnl.2020.125.

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Tesařová, Šárka, and Michal Vrablík. "New options in diagnostics and treatment of familial hypercholesterolemia." Medicína pro praxi 15, no. 3 (July 1, 2018): 122–26. http://dx.doi.org/10.36290/med.2018.026.

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Rosolová, Hana. "Advances of the contemporary treatment of hypertension and hypercholesterolemia by a new fixed combination." Vnitřní lékařství 68, no. 1 (February 14, 2022): 64–67. http://dx.doi.org/10.36290/vnl.2022.009.

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Gerritsen, Paola. "Minder diabetes type 2 bij familiaire hypercholesterolemie." Tijdschrift voor praktijkondersteuning 10, no. 3 (June 2015): 75–76. http://dx.doi.org/10.1007/s12503-015-0038-3.

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Boomsma, Louwrens, and Iris Kindt. "De praktijkondersteuner op zoek naar familiaire hypercholesterolemie." Tijdschrift voor praktijkondersteuning 2, no. 1 (February 2007): 19–24. http://dx.doi.org/10.1007/bf03074930.

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Vaclová, Martina, Tomáš Freiberger, Lucie Schwarzová, Lukáš Tichý, Michal Vrablík, and Richard Češka. "MedPed - the reality of familial hypercholesterolemia care at the biggest center." Vnitřní lékařství 64, no. 1 (January 1, 2018): 38–42. http://dx.doi.org/10.36290/vnl.2018.006.

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Soška, Vladimír, and Ondřej Kyselák. "Don't we forget about biological therapy of hypercholesterolemia with PCSK9-inhibitors?" Vnitřní lékařství 67, no. 3 (May 26, 2021): 138–42. http://dx.doi.org/10.36290/vnl.2021.034.

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Toll, P. J. M. M. "Pravastatine bij oudere patiënten met hypercholesterolemie en hypertensie." Medisch-Farmaceutische Mededelingen 42, no. 2 (February 2004): 32–33. http://dx.doi.org/10.1007/bf03058317.

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. "Screening op familiaire hypercholesterolemie: Preventie in de huisartsenpraktijk." Huisarts en Wetenschap 48, no. 11 (November 2005): 251–54. http://dx.doi.org/10.1007/bf03084213.

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. "NHG-Standpunt Diagnostiek en behandeling van familiaire hypercholesterolemie." Huisarts en Wetenschap 49, no. 4 (April 2006): 288. http://dx.doi.org/10.1007/bf03084705.

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JOOSEN H, VANDERSCHUEREN S, and BOBBAERS H. "Hypercholesterolemie bij bejaarden: is een behandeling met een statine zinvol?" Tijdschrift voor Geneeskunde 56, no. 22 (January 1, 2000): 1641–47. http://dx.doi.org/10.2143/tvg.56.22.5000901.

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PHILIPS H, VERMEIRE E, VAN ROYEN P, and DENEKENS J. "De kritische beoordeling van aanbevelingen voor de behandeling van hypercholesterolemie." Tijdschrift voor Geneeskunde 61, no. 5 (January 1, 2005): 335–45. http://dx.doi.org/10.2143/tvg.61.5.5002110.

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JOOSEN H, VANDERSCHUEREN S, and BOBBAERS H. "Hypercholesterolemie bij bejaarden: is een behandeling met een statine zinvol?" Tijdschrift voor Geneeskunde, no. 22 (January 1, 2000): 1641–47. http://dx.doi.org/10.47671/tvg.56.22.5000901.

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PHILIPS H, VERMEIRE E, VAN ROYEN P, and DENEKENS J. "De kritische beoordeling van aanbevelingen voor de behandeling van hypercholesterolemie." Tijdschrift voor Geneeskunde, no. 5 (January 1, 2005): 335–45. http://dx.doi.org/10.47671/tvg.61.5.5002110.

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Williams, P. Claire, Marcus J. Coffey, Barbara Coles, Stephanie Sanchez, Jason D. Morrow, John R. Cockcroft, Malcolm J. Lewis, and Valerie B. O'Donnell. "In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets." Blood 106, no. 8 (October 15, 2005): 2737–43. http://dx.doi.org/10.1182/blood-2005-02-0664.

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AbstractAntiplatelet therapies improve endothelial function in atherosclerosis, suggesting that platelets regulate vascular nitric oxide (NO) bioactivity in vivo. Herein, washed platelets consumed NO on activation in an aspirin-sensitive manner, and aspirin enhanced platelet NO responses in vitro. To examine whether in vivo aspirin can inhibit platelet NO consumption, a double-blind placebo-controlled study was conducted. After a 2-week nonsteroidal anti-inflammatory drug (NSAID)–free period, healthy men were randomly assigned and administered aspirin (75 mg/d orally) or identical placebo for 14 days, then crossed over to the opposite arm. Following in vivo aspirin, NO consumption by platelets was inhibited 91%. Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition. In a small substudy, NO consumption by platelets from postmenopausal women was faster in hypercholesterolemics and less sensitive to aspirin (ie, 39% versus 76% inhibition for hypercholesterolemics or normocholesterolemics, respectively). However, 150 mg aspirin/day increased inhibition of NO consumption by platelets of hypercholesterolemics to 80%. Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia. In conclusion, aspirin inhibits NO consumption by platelets from healthy subjects, but its beneficial effects on NO bioactivity may be compromised in some hypercholesterolemic patients.

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Venkadeswaran, Karuppasamy, Arumugam Ramachandran Muralidharan, Thangaraj Annadurai, Vasanthakumar Vasantha Ruban, Mahalingam Sundararajan, Ramalingam Anandhi, Philip A. Thomas, and Pitchairaj Geraldine. "Antihypercholesterolemic and Antioxidative Potential of an Extract of the Plant,Piper betle, and Its Active Constituent, Eugenol, in Triton WR-1339-Induced Hypercholesterolemia in Experimental Rats." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/478973.

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Hypercholesterolemia is a dominant risk factor for atherosclerosis and cardiovascular diseases. In the present study, the putative antihypercholesterolemic and antioxidative properties of an ethanolic extract ofPiper betleand of its active constituent, eugenol, were evaluated in experimental hypercholesterolemia induced by a single intraperitoneal injection of Triton WR-1339 (300 mg/kg b.wt) in Wistar rats. Saline-treated hypercholesterolemic rats revealed significantly higher mean blood/serum levels of glucose, total cholesterol, triglycerides, low density and very low density lipoprotein cholesterol, and of serum hepatic marker enzymes; in addition, significantly lower mean serum levels of high density lipoprotein cholesterol and significantly lower mean activities of enzymatic antioxidants and nonenzymatic antioxidants were noted in hepatic tissue samples from saline-treated hypercholesterolemic rats, compared to controls. However, in hypercholesterolemic rats receiving thePiper betleextract (500 mg/kg b.wt) or eugenol (5 mg/kg b.wt) for seven days orally, all these parameters were significantly better than those in saline-treated hypercholesterolemic rats. The hypercholesterolemia-ameliorating effect was better defined in eugenol-treated than inPiper betleextract-treated rats, being as effective as that of the standard lipid-lowering drug, lovastatin (10 mg/kg b.wt). These results suggest that eugenol, an active constituent of thePiper betleextract, possesses antihypercholesterolemic and other activities in experimental hypercholesterolemic Wistar rats.

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Luo, Ying, Quan-Neng Yan, Wan-Zhou Wu, and Fan-Yan Luo. "Decreased Count and Dysfunction of Circulating EPCs in Postmenopausal Hypercholesterolemic Females via Reducing NO Production." Stem Cells International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/2543847.

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Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.

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Rebolledo, Camilo, Alejandro Cuevas, Tomás Zambrano, Jacquelinne J. Acuña, Milko A. Jorquera, Kathleen Saavedra, Claudia Martínez, et al. "Bacterial Community Profile of the Gut Microbiota Differs between Hypercholesterolemic Subjects and Controls." BioMed Research International 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/8127814.

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The role of gut microbiota in the development of metabolic illnesses has been abundantly demonstrated. Recent studies suggest that gut microbiota alterations may also be related to the development of hypercholesterolemia. Therefore, we aimed to assess differences in the gut bacterial community profiles between hypercholesterolemic subjects and controls. Thirty cases diagnosed with hypercholesterolemia and 27 normocholesterolemic controls were included. A fasting whole blood sample was obtained to determine the lipid profile. In parallel, stool samples were collected and total DNA was isolated to assess the bacterial community profiles by denaturing gradient gel electrophoresis (DGGE). In addition, the Richness, Shannon-Weaver, and Simpson indexes were used to evaluate the richness and diversity of bacterial communities. As expected, serum concentrations of total cholesterol, triglycerides, and LDL-cholesterol were significantly higher in the cases compared with controls. Moreover, DGGE analysis showed a lower richness and diversity of bacterial communities in hypercholesterolemic subjects. In conclusion, our results showed differences in the profiles of bacterial communities between hypercholesterolemic subjects and controls, suggesting a possible role of the gut microbiota in the development of hypercholesterolemia.

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Trenteseaux, Charlotte, Anh-thu Gaston, Audrey Aguesse, Guillaume Poupeau, Pierre de Coppet, Ramaroson Andriantsitohaina, Jamila Laschet, et al. "Perinatal Hypercholesterolemia Exacerbates Atherosclerosis Lesions in Offspring by Altering Metabolism of Trimethylamine-N-Oxide and Bile Acids." Arteriosclerosis, Thrombosis, and Vascular Biology 37, no. 11 (November 2017): 2053–63. http://dx.doi.org/10.1161/atvbaha.117.309923.

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Objective— Experimental studies suggest that maternal hypercholesterolemia may be relevant for the early onset of cardiovascular disease in offspring. We investigated the effect of perinatal hypercholesterolemia on the atherosclerosis development in the offspring of apolipoprotein E–deficient mice and the underlying mechanism. Approach and Results— Atherosclerosis and related parameters were studied in adult male or female apolipoprotein E–deficient mice offspring from either normocholesterolemic or hypercholesterolemic mothers and normocholesterolemic fathers. Female born to hypercholesterolemic mothers had more aortic root lesions than female born to normocholesterolemic mothers. Lesions in whole aorta did not differ between groups. Higher trimethylamine-N-oxide levels and Fmo3 hepatic gene expression were higher in female born to hypercholesterolemic mothers offspring compared with female born to normocholesterolemic mothers and male. Trimethylamine-N-oxide levels were correlated with the size of atherosclerotic root lesions. Levels of hepatic cholesterol and gallbladder bile acid were greater in male born to hypercholesterolemic mothers compared with male born to normocholesterolemic mothers. At 18 weeks of age, female born to hypercholesterolemic mothers showed lower hepatic Scarb1 and Cyp7a1 but higher Nr1h4 gene expression compared with female born to normocholesterolemic mothers. Male born to hypercholesterolemic mothers showed an increase in Scarb1 and Ldlr gene expression compared with male born to normocholesterolemic mothers. At 25 weeks of age, female born to hypercholesterolemic mothers had lower Cyp7a1 gene expression compared with female born to normocholesterolemic mothers. DNA methylation of Fmo3, Scarb1 , and Ldlr promoter regions was slightly modified and may explain the mRNA expression modulation. Conclusions— Our findings suggest that maternal hypercholesterolemia may exacerbate the development of atherosclerosis in female offspring by affecting metabolism of trimethylamine-N-oxide and bile acids. These data could be explained by epigenetic alterations.

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Szabó, Márton Richárd, Márton Pipicz, Márta Sárközy, Bella Bruszel, Zoltán Szabó, and Tamás Csont. "Diet-Induced Hypercholesterolemia Leads to Cardiac Dysfunction and Alterations in the Myocardial Proteome." International Journal of Molecular Sciences 23, no. 13 (July 2, 2022): 7387. http://dx.doi.org/10.3390/ijms23137387.

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Elevated blood cholesterol is a major risk factor for coronary heart disease. Moreover, direct effects on the myocardium also contribute to the adverse effects of hypercholesterolemia. Here, we investigated the effect of hypercholesterolemia on the cardiac proteome. Male Wistar rats were fed with a laboratory rodent chow supplemented with 2% cholesterol for 8 weeks to induce hypercholesterolemia. The protein expression data obtained from the proteomic characterization of left ventricular samples from normo- and hypercholesterolemic animals were subjected to gene ontology (GO) and protein interaction analyses. Elevated circulating cholesterol levels were accompanied by diastolic dysfunction in cholesterol-fed rats. The proteomic characterization of left ventricular samples revealed altered expression of 45 proteins due to hypercholesterolemia. Based on the Gene Ontology analysis, hypercholesterolemia was associated with disturbed expression of cytoskeletal and contractile proteins. Beta-actin was downregulated in the hypercholesterolemic myocardium, and established a prominent hub of the protein interaction network. Analysis of the unfiltered dataset revealed concordant downregulated expression patterns in proteins associated with the arrangement of the contractile system (e.g., cardiac-specific troponins and myosin complex), and in subunits of the mitochondrial respiratory chain. We conclude that the observed changes in the cardiac proteome may contribute to the development of diastolic dysfunction in hypercholesterolemia.

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Viola, Sheila, Pascale Benlian, Alain Morali, Dries Dobbelaere, Florence Lacaille, Daniel Rieu, Jean Louis Ginies, et al. "Apolipoprotein B Arg3500Gln Mutation Prevalence in Children With Hypercholesterolemia: A French Multicenter Study." Journal of Pediatric Gastroenterology and Nutrition 33, no. 2 (August 2001): 122–26. http://dx.doi.org/10.1002/j.1536-4801.2001.tb07422.x.

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ABSTRACTBackgroundFamilial defective apolipoprotein B‐100, a dominantly inherited form of hypercholesterolemia caused by a single Arg3500Gln mutation, is silent in childhood but may confer a high risk of cardiovascular disease in adulthood. The objective was to determine the prevalence of familial defective apolipoprotein B‐100 in hypercholesterolemic French children and to provide a basis for targeting screening efforts in this population.MethodsOne hundred ninety children attending 13 pediatric clinics distributed throughout France were included based on the presence of type IIa hypercholesterolemia with a plasma low‐density lipoprotein–cholesterol level of more than 130 mg/dL. The Arg3500Gln mutation was detected in dried blood spots using a polymerase chain reaction assay combined with enzymatic restriction.ResultsThree hyperlipidemia phenotypes were found: monogenic dominant pure hypercholesterolemia (n = 117), polygenic hypercholesterolemia (n = 43), and combined hyperlipidemia (n = 11). Three unrelated children were heterozygous for the Arg3500Gln mutation; all three had monogenic dominant pure hypercholesterolemia (3/94 families; 3.2%), yielding a prevalence of 1.83% (3/164) in hypercholesterolemic children, which is similar to prevalences reported in European adults.ConclusionsThe familial defective apolipoprotein B‐100 mutation was common (1/31) in children with a phenotype of familial hypercholesterolemia, supporting screening in this population with the goal of preventing premature cardiovascular events.

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Harris, N. R., and D. N. Granger. "Neutrophil enhancement of reperfusion-induced capillary fluid filtration associated with hypercholesterolemia." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H1755—H1761. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h1755.

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Fluid filtration rate (Jv/S) from individual mesenteric capillaries in normocholesterolemic and hypercholesterolemic rats was measured before and after 30 min each of ischemia and reperfusion (I/R). The median I/R-induced increase in Jv/S (I/R vs. baseline) was 44% in normocholesterolemic rats (n = 11) and 97% in hypercholesterolemic rats (n = 11). A positive correlation slope of 0.20% per mg/dl resulted when the percent Jv/S increase vs. plasma cholesterol concentration (P = 0.02) was plotted, demonstrating that hypercholesterolemia enhances the capillary response to I/R. Because microvascular pressure did not change significantly after I/R in either group of rats, the increments in Jv/S likely reflect increased capillary permeability. In hypercholesterolemic rats rendered neutropenic with antineutrophil serum, I/R did not elicit a significant increase in Jv/S, suggesting that activated neutrophils mediate the exaggerated endothelial barrier dysfunction associated with hypercholesterolemia.

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Mohd Yahaya, Noor Fazila, Norhaniza Aminudin, and Noorlidah Abdullah. "Effectuation of Pleurotus pulmonarius on Hypercholesterolemic Wistar-Kyoto Rats: Analysis on Liver and Sera." Sains Malaysiana 51, no. 11 (November 30, 2021): 3755–64. http://dx.doi.org/10.17576/jsm-2022-5111-19.

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Hypercholesterolemia is one of the potential risks of cardiovascular heart disease (CHD). An early diagnosis and treatment attenuate the risk of CHD. Besides statin prescription for hypercholesterolemia, functional food has an added value to ameliorate the risk. This study was conducted to analyse the significant effect of grey oyster mushroom (Pleurotus pulmonarius) on hypercholesterolemia. Thirty-six Wistar-Kyoto rats were assigned into six groups, consisted of normal (N), hypercholesterolemia (H), two groups for prevention (P1 and P2), and two groups for treatment (T1 and T2). For prevention purpose, P1 and P2 were concomitantly induced to be hypercholesterolemic and fed with either crude aqueous extract of P. pulmonarius (CA) or simvastatin for 45 days. Following 45 days of hypercholesterolemic-induction, T1 and T2 rats were then orally fed with either CA or simvastatin for another 30 days. On day 45, groups N, H, P1, and P2 were sacrificed, whereas groups T1 and T2 were sacrificed on day 75. Histopathology examination showed the conditions of liver tissues. Fat droplets were observed in hypercholesterolemic hepatic tissues and were also remained in the hepatic tissues of rats belonged to the treatment groups. The tissues’ viability was better in prevention groups suggesting the compound(s) present in CA might be able to protect them from further damage. Metabolomic analysis of the sera from P1 and T1 rats showed altered regulation of several metabolites such as pantothenic acid, N-carbamylglutamate, serotonin and ceramide against the control group.

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Kim, Joungyoun, Hyeong-Seop Kim, Woojung Yang, Jae-woo Lee, and Hee-Taik Kang. "Primary Prevention of Cardiocerebrovascular Diseases and Related Deaths According to Statin Type." International Journal of Environmental Research and Public Health 17, no. 17 (August 30, 2020): 6309. http://dx.doi.org/10.3390/ijerph17176309.

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(1) Background: Statin is the mainstay of treatment for the primary prevention of atherosclerotic cardiocerebrovascular diseases (CCVDs) in adults with hypercholesterolemia. This study aims to investigate the differences in effect on primary composite outcomes (CCVDs and CCVD-related deaths) among five statins in hypercholesterolemic individuals. (2) Methods: This retrospective study is based on the Korean National Health Insurance Service-National Health Screening Cohort. Participants, aged 40 to 69 years at baseline, were categorized into five statin-treated groups (pitavastatin, atorvastatin, rosuvastatin, simvastatin, and pravastatin) and two untreated groups (untreated hypercholesterolemia and no hypercholesterolemia). (3) Results: A total of 161,583 individuals was included. The median follow-up period was 8.2 years. Compared with the pitavastatin group, the hazard ratios (HRs; 95% confidence intervals (CIs)) for CCVDs and CCVD-related deaths of the atorvastatin, rosuvastatin, simvastatin, pravastatin, untreated hypercholesterolemia, and no-hypercholesterolemia groups were 0.969 (0.567–1.657), 0.988 (0.533–1.832), 0.862 (0.490–1.518), 0.906 (0.326–2.515), 2.665 (1.556–4.562), and 0.656 (0.388–1.110), respectively, in men and 1.124 (0.632–1.999), 1.119 (0.582–2.152), 1.324 (0.730–2.400), 1.023 (0.330–3.171), 2.650 (1.476–4.758), and 0.921 (0.522–1.625), respectively, in women, after being fully adjusted. (4) Conclusions: No significant differences among the five statins were observed, but there was an increased risk in untreated hypercholesterolemic individuals, for CCVDs and CCVDs-related deaths in individuals with hypercholesterolemia of either sex.

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Saaty, Afnan H. "Achillea Fragrantissima Ethanolic Extract Exerts Hypocholesterolemia and Hepatic Antioxidant Effects in High Fat-Cholesterol Diet: An Experimental Study." Pakistan Journal of Medical and Health Sciences 15, no. 11 (November 30, 2021): 3406–10. http://dx.doi.org/10.53350/pjmhs2115113406.

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Background: Hypercholesterolemia and oxidative stress consider the main causes for atherosclerotic cardiovascular diseases, that are one of the major non-communicable diseases responsible for more than a third of deaths in Saudi Arabia. Cholesterol-lowering medications as Atorvastatin® (ATOR) are linked to a variety of side effects. Achillea fragarntissima (AF) is a valuable medicinal plant in Saudi Arabia with potent antioxidant activity. Aim: The current study was performed to determine the efficacy of AF in the treatment of hypercholesterolemia through the antioxidant metabolic pathway. Methodology: Dried aerial parts of AF were extracted by ethanol (70%). Induction of hypercholesterolemia in rats was induced through feeding a high fat-cholesterol diet (HFCD) for 8 weeks. Rats were assigned to two main groups; control group (Cont, n=10) rats fed a standard diet, and hypercholesterolemic group (HFCD) (n=40) rats fed HFCD. The HFCD group was further assigned after measured lipid profile to confirm the induction of hypercholesterolemia to HFCD; HFCD+AF (hypercholesterolemic rats treated orally with 500 mg/kg AF); HFCD+ ATOR (hypercholesterolemic rats treated orally with 20 mg/kg ATOR, as a reference drug); and HFCD+AF+ATOR (hypercholesterolemic rats treated orally with AF+ ATOR). Different treatments were ingested to rats for 4 weeks. Results: The results revealed that the HFCD group showed significant hyperlipidemia (elevation of serum TC, TG, LDL-C, and VLDL-C levels concurrent with a reduction in serum HDL-C level); significant disturbance in liver functions (elevation in serum ALT, AST, and ALP enzymes activities); and significant oxidative stress (elevation in hepatic MDA level with a reduction in hepatic SOD activity) compared with the Cont group. Besides, hepatic central vein section showed deposition of large lipid within hepatocytes and abundant focal cell necrosis. Oral treatment with AF, ATOR, and the mixture of the drug and AF produced significant hypocholesterolemia, antioxidant, and improved liver function enzymes, with normalized hepatic central vein tissue compared with the HFCD group. The mixture of AF+ATOR had a superior effect than either treatment alone. Conclusion: In hypercholesterolemic rats, AF may be used to prevent atherosclerosis through improving lipid profile levels, protecting against hepatic oxidative stress, and ameliorating hepatic functions. Thus highlighting its valuable effects in the treatment of atherosclerotic cardiovascular diseases. Keywords: Achillea fragarntissima, lipid profile, hepatic oxidative stress, hepatic function, hypercholesterolemia.

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Bláha, Vladimír, Milan Bláha, Miriam Lánská, Eduard Havel, Pavel Vyroubal, Zdeněk Zadák, and Pavel Žák. "The role of PCSK9-inhibitors and of lipoprotein apheresis in the treatment of homozygous and severe heterozygous familial hypercholesterolemia: A rivalry, or are things quite different?" Vnitřní lékařství 64, no. 1 (January 1, 2018): 43–50. http://dx.doi.org/10.36290/vnl.2018.007.

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Lidesna Shinta Amat, Anita, Herman Pieter Louis Wungouw, Efrisca Meliyuita Br Damanik, Prisca Pakan, and Desi Indriarini. "Ethanolic extract of Muntingia calabura L. as an antihypercholesterolemic by reducing malondialdehyde (MDA) levels in white mice (Mus musculus)." Biomedicine 43, no. 5 (November 8, 2023): 1443–46. http://dx.doi.org/10.51248/.v43i5.2881.

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Introduction and Aim: A diet high in cholesterol causes hypercholesterolemia by elevating plasma cholesterol levels. Hypercholesterolemia causes an increase in cholesterol concentration within cells, resulting in membrane-altering lipid peroxidation. Malondialdehyde (MDA) is produced during lipid peroxidation to form peroxides and other free radicals. The present study aims to evaluate the potential of Muntingia calabura L. ethanolic extracts as a hypercholesterolemia agent by reducing MDA levels in hypercholesterolemic white mice (Mus musculus). Materials and Methods: The present study has a true experimental design with a control group consisting only of post-test samples. The research utilized approximately 25 white mice (Mus musculus) randomly. These white mice were separated into five groups, consists of negative control (C1), positive control (C2), M. calabura L. ethanolic extracts at doses of 13 mg/20g/BW (C3), 26 mg/20g/BW (C4), and 52mg/20g/BW (C5). The concentration of MDA was measured on the 21st day of treatment using the TBARS method. Results: The results indicated that the M. calabura L. extracts significantly (p<0.05) reduce the total cholesterol and MDA levels in the blood of white mice (Mus musculus). The evidence supporting this conclusion is based on the data obtained from mice that received various doses of M. calabura L leaf extract, specifically 13mg/20g/BW, 26mg/20g/BW, and 52mg/20g/BW. These doses already demonstrated a substantial reduction in MDA levels following the treatment. Conclusion: In this research, it was found that the ethanolic extract of M. calabura L leaves effectively acted as an anti-hypercholesterolemic agent in mice with hypercholesterolemia. The assessment of its anti-hypercholesterolemic properties was based on the observation of reduced MDA levels. It is suggested that the leaf extract of M. calabura L contains a compound known as phytol, which is believed to have the capacity to inhibit hypercholesterolemia in white mice (Mus musculus).

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Heaps, C. L., D. L. Tharp, and D. K. Bowles. "Hypercholesterolemia abolishes voltage-dependent K+ channel contribution to adenosine-mediated relaxation in porcine coronary arterioles." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (February 2005): H568—H576. http://dx.doi.org/10.1152/ajpheart.00157.2004.

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Hypercholesterolemic patients display reduced coronary flow reserve in response to adenosine infusion. We previously reported that voltage-dependent K+ (Kv) channels contribute to adenosine-mediated relaxation of coronary arterioles isolated from male miniature swine. For this study, we hypothesized that hypercholesterolemia attenuates Kv channel contribution to adenosine-induced vasodilatation. Pigs were randomly assigned to a control or high fat/high cholesterol diet for 20–24 wk, and then killed. After completion of the experimental treatment, arterioles (∼150 μm luminal diameter) were isolated from the left-ventricular free wall near the apical region of the heart, cannulated, and pressurized at 40 mmHg. Adenosine-mediated relaxation was significantly attenuated in both endothelium-intact and -denuded arterioles from hypercholesterolemic compared with control animals. The classic Kv channel blocker, 4-aminopyridine (1 mM), significantly attenuated adenosine-mediated relaxation in arterioles isolated from control but not hypercholesterolemic animals. Furthermore, the nonselective K+ channel blocker, tetraethylammonium (TEA; 1 mM) significantly attenuated adenosine-mediated relaxation in arterioles from control but not hypercholesterolemic animals. In additional experiments, coronary arteriolar smooth muscle cells were isolated, and whole cell K v currents were measured. Kv currents were significantly reduced (∼15%) in smooth muscle cells from hypercholesterolemic compared with control animals. Furthermore, Kv current sensitive to low concentrations of TEA was reduced (∼45%) in smooth muscle cells from hypercholesterolemic compared with control animals. Our data indicate that hypercholesterolemia abolishes Kv channel contribution to adenosine-mediated relaxation in coronary arterioles, which may be attributable to a reduced contribution of TEA-sensitive K v channels in smooth muscle of hypercholesterolemic animals.

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Caselato-Sousa, Valeria Maria, Michiko Regina Ozaki, Eros Antonio de Almeida, and Jaime Amaya-Farfan. "Intake of heat-expanded amaranth grain reverses endothelial dysfunction in hypercholesterolemic rabbits." Food Funct. 5, no. 12 (2014): 3281–86. http://dx.doi.org/10.1039/c4fo00468j.

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Feeding amaranth grain to hypercholesterolemic rabbits showed the property of recovering the lost endothelial function even without removing the hypercholesterolemia-inducing diet. Results suggest an underlying protective effect.

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Jafari, Sima, Farah Farokhi, and Abbas Sadeghi. "Comparative effects of garlic (Allium sativum) powder and atorvastatin in female reproductive system of hypercholesterolemic rats: A histological and biochemical evaluation." Journal of Shahrekord University of Medical Sciences 23, no. 3 (September 29, 2021): 131–38. http://dx.doi.org/10.34172/jsums.2021.22.

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Background and aims: The abnormal increase in blood cholesterol can cause many problems. Statins have a cholesterol-lowering effect, but they also have adverse effects. Garlic prevents the formation of cholesterol due to its antibiotic properties. This study aimed to investigate the comparative effect of garlic powder and atorvastatin on hypercholesterolemia-induced reproductive failure in female rats. Methods: In the present experimental study, 48 adult female Wistar rats were divided into eight groups (n=6), including control, atorvastatin (10 mg/kg/d; orally), atorvastatin (20 mg/kg/d; orally), garlic powder (100 mg/kg/d; orally), hypercholesterolemia (1.5 mg/kg/d of cholesterol; orally), hypercholesterolemia + atorvastatin (10 mg/kg/d), hypercholesterolemia + atorvastatin (20 mg/kg/d), and hypercholesterolemia + garlic powder. After 30 days, rats were euthanized and blood samples were obtained from their heart for serological assessments. The right ovary was transferred to 10% formalin for histological analyses, and the left ovary was transferred to a −80°C freezer for evaluation of oxidative stress markers. Data were statistically analyzed by ANOVA and Tukey’s test using SPSS version 24.0 (P<0.05). Results: The number of healthy primordial, primary, secondary, and antral follicles, catalase activity, total antioxidant capacity (TAOC) as well as estrogen and progesterone levels were lower in hypercholesterolemic rats compared to controls (P<0.001). Additionally, the number of the atretic primary, secondary, and antral follicles and malondialdehyde (MDA) levels were higher in hypercholesterolemic rats (P<0.001). However, garlic powder and atorvastatin 10 improved alterations in the mentioned parameters (P=0.99). Conclusion: The results showed that hypercholesterolemia could have adverse effects on rat ovaries. However, the garlic powder improves ovarian toxicity in hypercholesterolemia rats better than atorvastatin.

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de Oliveira, Jade, Daiane F. Engel, Gabriela C. de Paula, Danúbia B. dos Santos, Jadna B. Lopes, Marcelo Farina, Eduardo L. G. Moreira, and Andreza F. de Bem. "High Cholesterol Diet Exacerbates Blood-Brain Barrier Disruption in LDLr–/– Mice: Impact on Cognitive Function." Journal of Alzheimer's Disease 78, no. 1 (October 27, 2020): 97–115. http://dx.doi.org/10.3233/jad-200541.

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Background: Evidence has revealed an association between familial hypercholesterolemia and cognitive impairment. In this regard, a connection between cognitive deficits and hippocampal blood-brain barrier (BBB) breakdown was found in low-density lipoprotein receptor knockout mice (LDLr–/–), a mouse model of familial hypercholesterolemia. Objective: Herein we investigated the impact of a hypercholesterolemic diet on cognition and BBB function in C57BL/6 wild-type and LDLr–/–mice. Methods: Animals were fed with normal or high cholesterol diets for 30 days. Thus, wild-type and LDLr–/–mice were submitted to memory paradigms. Additionally, BBB integrity was evaluated in the mice’s prefrontal cortices and hippocampi. Results: A tenfold elevation in plasma cholesterol levels of LDLr–/–mice was observed after a hypercholesterolemic diet, while in wild-type mice, the hypercholesterolemic diet exposure increased plasma cholesterol levels only moderately and did not induce cognitive impairment. LDLr–/–mice presented memory impairment regardless of the diet. We observed BBB disruption as an increased permeability to sodium fluorescein in the prefrontal cortices and hippocampi and a decrease on hippocampal claudin-5 and occludin mRNA levels in both wild-type and LDLr–/–mice treated with a hypercholesterolemic diet. The LDLr–/–mice fed with a regular diet already presented BBB dysfunction. The BBB-increased leakage in the hippocampi of LDLr–/–mice was related to high microvessel content and intense astrogliosis, which did not occur in the control mice. Conclusion: Therefore, LDLr–/–mice seem to be more susceptible to cognitive impairments and BBB damage induced by exposure to a high cholesterol diet. Finally, BBB disruption appears to be a relevant event in hypercholesterolemia-induced brain alterations.

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Maas, Renke, Edzard Schwedhelm, Lydia Kahl, Huige Li, Ralf Benndorf, Nicole Lüneburg, Ulrich Förstermann, and Rainer H. Böger. "Simultaneous Assessment of Endothelial Function, Nitric Oxide Synthase Activity, Nitric Oxide–Mediated Signaling, and Oxidative Stress in Individuals with and without Hypercholesterolemia." Clinical Chemistry 54, no. 2 (February 1, 2008): 292–300. http://dx.doi.org/10.1373/clinchem.2007.093575.

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Abstract Background: Endothelial function is impaired in hypercholesterolemia and atherosclerosis. Based on mostly indirect evidence, this impairment is attributed to reduced synthesis or impaired biological activity of endothelium-derived nitric oxide (NO). It was the aim of this study to directly estimate and compare whole-body NO production in normo- and hypercholesterolemia by applying a nonradioactive stable isotope dilution technique in vivo. Methods: We enrolled 12 normocholesterolemic and 24 hypercholesterolemic volunteers who were all clinically healthy. To assess whole-body NO synthesis, we intravenously administered l-[guanidino-(15N2)]-arginine and determined the urinary excretion of 15N-labeled nitrate, the specific end product of NO oxidation in humans, by use of gas chromatography-mass spectrometry. In addition, we measured flow-mediated vasodilation (FMD) of the brachial artery, expression of endothelial NOS (eNOS) in platelets, plasma concentration of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), and urinary excretion of 8-isoprostaglandin F2α (8-iso-PGF2α). Results: After infusion of l-[guanidino-(15N2)]-arginine, cumulative excretion of 15N-labeled-nitrate during 48 h was 40% [95% CI 15%–66%] lower in hypercholesterolemic than normocholesterolemic volunteers [mean 9.2 (SE 0.8) μmol vs 15.4 (2.3) μmol/l, P = 0.003]. FMD was on average 36% [4%–67%] lower in hypercholesterolemic than normocholesterolemic volunteers [6.3 (4.0)% vs 9.4 (4.6)%, P = 0.027]. Normalized expression of NOS protein in platelets was also significantly lower in hypercholesterolemic volunteers, whereas there were no significant differences in plasma ADMA concentration or urinary excretion of 8-iso-PGF2α between the 2 groups. Conclusions: This study provides direct evidence for a decreased whole body NO synthesis rate in healthy people with hypercholesterolemia.

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Chan, Kim Wei, Maznah Ismail, Norhaizan Mohd Esa, Noorjahan Banu Mohamed Alitheen, Mustapha Umar Imam, Der Jiun Ooi, and Nicholas M. H. Khong. "Defatted Kenaf (Hibiscus cannabinus L.) Seed Meal and Its Phenolic-Saponin-Rich Extract Protect Hypercholesterolemic Rats against Oxidative Stress and Systemic Inflammation via Transcriptional Modulation of Hepatic Antioxidant Genes." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/6742571.

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The present study aimed to investigate the antioxidant and anti-inflammatory properties of defatted kenaf seed meal (DKSM) and its phenolic-saponin-rich extract (PSRE) in hypercholesterolemic rats. Hypercholesterolemia was induced using atherogenic diet feeding, and dietary interventions were conducted by incorporating DKSM (15% and 30%) or PSRE (at 2.3% and 4.6%, resp., equivalent to the total content of DKSM-phenolics and saponins in the DKSM groups) into the atherogenic diets. After ten weeks of intervention, serum total antioxidant capacities of hypercholesterolemic rats were significantly enhanced by DKSM and PSRE supplementation (p<0.05). Similarly, DKSM and PSRE supplementation upregulated the hepatic mRNA expression of antioxidant genes (Nrf2, Sod1, Sod2, Gsr, and Gpx1) of hypercholesterolemic rats (p<0.05), except for Gpx1 in the DKSM groups. The levels of circulating oxidized LDL and proinflammatory biomarkers were also markedly suppressed by DKSM and PSRE supplementation (p<0.05). In aggregate, DKSM and PSRE attenuated the hypercholesterolemia-associated oxidative stress and systemic inflammation in rats, potentially by enhancement of hepatic endogenous antioxidant defense via activation of the Nrf2-ARE pathway, which may be contributed by the rich content of phenolics and saponins in DKSM and PSRE. Hence, DKSM and PSRE are prospective functional food ingredients for the potential mitigation of atherogenic risks in hypercholesterolemic individuals.

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El Rabey, Haddad A., Madeha N. Al-Seeni, and Habibah B. Al-Ghamdi. "Comparison between the Hypolipidemic Activity of Parsley and Carob in Hypercholesterolemic Male Rats." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/3098745.

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Hypercholesterolemia is commonly associated with obesity that leads to heart diseases and diabetes. The hepatocardioprotective activity of parsley and carob methanol extract was tested in hypercholesterolemic male rats. Twenty-four male albino rats were divided into four groups (n=6). Group 1 was the negative control group fed with fat rich diet, group 2 (G2) was hypercholesterolemic rats fed with fat rich diet with 2% cholesterol, and group 3 and group 4 (G3 and G4) were hypercholesterolemic rats supplemented with 2% cholesterol and cotreated with 20% w/w parsley seed methanol extract and 20% w/w carob legume methanol extract, respectively. The experiment was conducted for eight weeks. The positive hypercholesterolemic rats showed significant increase in serum levels of total cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), lactate dehydrogenase (LDH), creatine kinase-mb, liver function enzymes, and decrease in the high density lipoproteins (HDL). Moreover, heart and liver tissues were ameliorated and nearly restored their normal appearance. It could be concluded that both parsley and carob extracts supplementations have a protective effect against hyperlipidemia and improved the histological alteration in heart and liver tissues. The methanol extract of parsley appeared to be more efficient than that of carob in lowering hypercholesterolemia.

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Kim, Min-ho, Patsy R. Carter, and Norman R. Harris. "P-selectin-mediated adhesion impairs endothelium-dependent arteriolar dilation in hypercholesterolemic mice." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H632—H638. http://dx.doi.org/10.1152/ajpheart.00780.2006.

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Hypercholesterolemia is associated with an attenuation of endothelium-dependent dilation in arterioles and an increase in leukocyte and platelet adhesion in venules. The proximity of closely paired arterioles and venules is thought to facilitate heat and mass transport between the two and could be involved in transport of inflammatory and/or vasoactive mediators from venule to arteriole. In the current study, we tested the hypothesis that the impaired arteriolar dilation associated with hypercholesterolemia might be dependent on P-selectin-dependent blood cell adhesion in the closely paired venules. Leukocyte and platelet recruitment in venules and the endothelium-dependent response to bradykinin in second-order arterioles were observed in the mouse intestinal submucosa using intravital microscopy. Four weeks of a high-cholesterol diet decreased bradykinin-induced arteriolar dilation more dramatically in closely paired arterioles than in distantly paired arterioles. The dysfunctional arteriolar dilation of closely paired arterioles in hypercholesterolemic mice was significantly improved when the experiments were repeated in P-selectin-deficient mice (given the high-cholesterol diet) or in hypercholesterolemic mice injected with a P-selectin monoclonal antibody. A similar improvement in dilation of closely paired arterioles was attained in hypercholesterolemic mice given the superoxide dismutase mimetic Tempol. These findings indicate that hypercholesterolemia-induced increases in venular leukocyte and platelet adhesion might contribute to the impaired endothelium-dependent dilation of closely paired arterioles via a mechanism that is distance limited and dependent on P-selectin and superoxide.

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Szabó, Márton R., Renáta Gáspár, Márton Pipicz, Nóra Zsindely, Petra Diószegi, Márta Sárközy, László Bodai, and Tamás Csont. "Hypercholesterolemia Interferes with Induction of miR-125b-1-3p in Preconditioned Hearts." International Journal of Molecular Sciences 21, no. 11 (May 26, 2020): 3744. http://dx.doi.org/10.3390/ijms21113744.

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Ischemic preconditioning (IPre) reduces ischemia/reperfusion (I/R) injury in the heart. The non-coding microRNA miR-125b-1-3p has been demonstrated to play a role in the mechanism of IPre. Hypercholesterolemia is known to attenuate the cardioprotective effect of preconditioning; nevertheless, the exact underlying mechanisms are not clear. Here we investigated, whether hypercholesterolemia influences the induction of miR-125b-1-3p by IPre. Male Wistar rats were fed with a rodent chow supplemented with 2% cholesterol and 0.25% sodium-cholate hydrate for 8 weeks to induce high blood cholesterol levels. The hearts of normo- and hypercholesterolemic animals were then isolated and perfused according to Langendorff, and were subjected to 35 min global ischemia and 120 min reperfusion with or without IPre (3 × 5 min I/R cycles applied before index ischemia). IPre significantly reduced infarct size in the hearts of normocholesterolemic rats; however, IPre was ineffective in the hearts of hypercholesterolemic animals. Similarly, miR-125b-1-3p was upregulated by IPre in hearts of normocholesterolemic rats, while in the hearts of hypercholesterolemic animals IPre failed to increase miR-125b-1-3p significantly. Phosphorylation of cardiac Akt, ERK, and STAT3 was not significantly different in any of the groups at the end of reperfusion. Based on these results we propose here that hypercholesterolemia attenuates the upregulation of miR-125b-1-3p by IPre, which seems to be associated with the loss of cardioprotection.

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Soliman, Ghada Z. A. "Effect of Wheat Germ, Wheat Germ Oil on Lipid Profile of Hypercholesterolemic Rats." International Journal of Lipids 1, no. 1 (December 25, 2020): 11–20. http://dx.doi.org/10.14302/issn.2835-513x.ijl-20-3247.

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Hypercholesterolemia plays an important role in atherosclerosis and cardiovascular diseases (CVD) that represent one of the greatest worldwide medical problems nowadays. Recently, an increased attention/ interest for natural antioxidant/ hypercholesterolemia as WG/WGO is increasing. Wheat germ/ Wheat germ oil (WG/WGO) is an excellent source of essential and polyunsaturated fatty acids and vitamin E. It is one of the richest natural sources of tocopherol. This work aims to evaluate the effect of administration of wheat germ (WG) /wheat germ oil (WGO) for 6 weeks on serum lipid profile, lipid peroxidation (liver malondialdehyde) in hypercholesterolemic rats. One hundred and twenty maleSprague Dawelyrats weighing 180-192 gm were used in this study. They were randomly distributed into six groups (20 rats/ group) as follow: g1: normal control, G2: hypercholesterolemic rats; G3: Normal rats treated with WG; G4: hypercholesterolemic rats treated with WG; G5: Normal rats treated with WGO; G6: hypercholesterolemic rats treated with WGO for 6 weeks. Also WG was analysed for its nutritive value, while WGO was analysed for fatty acid profile, and studied for its physico-chemical properties. The results showed significant elevation of liver malondialdehyde (MDA) and serum lipid profile in untreated rats fed on hypercholesterolemic diet. Hypercholesterolemic rats treated with WG/WGO showed an improvement in the biochemical assay of their lipid profile compared with untreated hypercholesterolemic rats. WG/WGO may be able to protect against atherosclerosis and CVD. The administration of WG /WGO to diets of rats caused a marked reduction in TC, LDL-C, VLDL-C, TG and MDA. This improvement effect may be mediated via enhancement of the antioxidant defence system and other factors. However, further clinical studies on human beings are required to assess the efficacy and safety of the WG/WGO.

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Gömöri, Kamilla, Tamara Szabados, Éva Kenyeres, Judit Pipis, Imre Földesi, Andrea Siska, György Dormán, Péter Ferdinandy, Anikó Görbe, and Péter Bencsik. "Cardioprotective Effect of Novel Matrix Metalloproteinase Inhibitors." International Journal of Molecular Sciences 21, no. 19 (September 23, 2020): 6990. http://dx.doi.org/10.3390/ijms21196990.

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Background: We recently developed novel matrix metalloproteinase-2 (MMP-2) inhibitor small molecules for cardioprotection against ischemia/reperfusion injury and validated their efficacy in ischemia/reperfusion injury in cardiac myocytes. The aim of the present study was to test our lead compounds for cardioprotection in vivo in a rat model of acute myocardial infarction (AMI) in the presence or absence of hypercholesterolemia, one of the major comorbidities affecting cardioprotection. Methods: Normocholesterolemic adult male Wistar rats were subjected to 30 min of coronary occlusion followed by 120 min of reperfusion to induce AMI. MMP inhibitors (MMPI)-1154 and -1260 at 0.3, 1, and 3 µmol/kg, MMPI-1248 at 1, 3, and 10 µmol/kg were administered at the 25th min of ischemia intravenously. In separate groups, hypercholesterolemia was induced by a 12-week diet (2% cholesterol, 0.25% cholic acid), then the rats were subjected to the same AMI protocol and single doses of the MMPIs that showed the most efficacy in normocholesterolemic animals were tested in the hypercholesterolemic animals. Infarct size/area at risk was assessed at the end of reperfusion in all groups by standard Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) staining, and myocardial microvascular obstruction (MVO) was determined by thioflavine-S staining. Results: MMPI-1154 at 1 µmol/kg, MMPI-1260 at 3 µmol/kg and ischemic preconditioning (IPC) as the positive control reduced infarct size significantly; however, this effect was not seen in hypercholesterolemic animals. MVO in hypercholesterolemic animals decreased by IPC only. Conclusions: This is the first demonstration that MMPI-1154 and MMPI-1260 showed a dose-dependent infarct size reduction in an in vivo rat AMI model; however, single doses that showed the most efficacy in normocholesterolemic animals were abolished by hypercholesterolemia. The further development of these promising cardioprotective MMPIs should be continued with different dose ranges in the study of hypercholesterolemia and other comorbidities.

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Journal articles on the topic 'Hypercholesterolemie'

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