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Zocor (Simvastatin)

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Zocor is an HMG-CoA reductase inhibitor. Zocor is used to reduce the risk of heart attack, stroke, and death due to coronary heart disease. It also reduces the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina, it lows high cholesterol and triglycerides and increases high-density lipoprotein (HDL, "good") cholesterol levels. Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Other names for this medication:

Similar Products:
Crestor, Zetia, Tricor, Pravachol, Mevacor, Lipitor


Also known as:  Simvastatin.


Zocor is an HMG-CoA reductase inhibitor.

Zocor is used to: reduce the risk of heart attack, stroke, and death due to coronary heart disease; reduce the risk of heart attack, stroke, blood vessel blockage, or chest pain caused by angina; low high cholesterol and triglycerides; increase high-density lipoprotein (HDL, "good") cholesterol levels.

Zocor is also known as Imvastatin, Simlup, Simcardis, Ranzolont, Simvador.

Zocor works by reducing the production of certain fatty substances in the body, including cholesterol.

Generic name of Zocor is Simvastatin.

Brand name of Zocor is Zocor.


Take Zocor orally.

Take Zocor with or without food.

Do not use grapefruit or grapefruit juice while taking Zocor. Eating grapefruit or drinking grapefruit juice may increase the amount of Zocor in blood, what may increase the serious side effects.

If you want to achieve most effective results do not stop taking Zocor suddenly.


If you overdose Zocor and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zocor are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Zocor if you are allergic to Zocor components.

Be careful with Zocor if you're pregnant or you plan to have a baby. Do not use it if you are a nursing mother.

Be careful with Zocor if you suffer from low blood pressure, kidney problems, diabetes, serious infection, metabolism problems, hormonal problems.

Do not use potassium supplements or salt substitutes.

Avoid eating grapefruit or drinking grapefruit juice while taking Zocor.

While taking Zocor, you can make laboratory tests (blood cholesterol levels, liver function tests, creatine phosphokinase blood levels) to monitor the condition of your health.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Be very careful when you are driving machine.

Do not stop taking Zocor suddenly.

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Ten 30-week-old rats received pure titanium implants in both tibiae, and were then divided into experimental and control groups. The experimental group was administered simvastatin daily. Thirty days later, all animals were killed and then specimens were prepared. The bone contact ratio (BCR) to the implant and bone density (BD) around the implant, as well as histological findings, were obtained.

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20 male Wistar Albino rats weighing 230-250 gr were used. The rats were housed for 12 hours day and 12 hours night cycles in cages and were divided into two groups, namely study and control group. Microscopic evaluation of adhesion was assessed under 5 main topics which are the signs of inflammatory response; inflammation, activation, fibroblast activity, vascularity, presence of giant cell. Activation was scored as follows: (0) no activation, (1) while activation was accepted as present the score for other parameters was evaluated between 0 to 3 according to the increased severity. After evaluating all topics separately, the average of all scores has been assessed in both groups.

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Compared with the model group, serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), MDA, and atherosclerotic index (AI) were significantly lowered in the MZTC groups (P<0.05, P<0.01), while serum levels of high-density lipoprotein cholesterol (HDL-C), SOD, and NO obviously increased (P<0.05, P<0.01). Serum levels of TC, TG, LDL-C, and in the MZTC groups were obviously higher than those of the simvastatin group (P<0.01), and there was insignificant difference in other indices. The ratio of the aortic tunica intima plaque percentage to the total tunica intima area was also markedly lower than that of the model group (P<0.05, P<0.01). Results under light microscope indicated the pathological changes of the aorta was obviously attenuated.

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Simvastatin (SMV) has been shown to exhibit promising anti-inflammatory properties alongside its classic cholesterol lowering action. We tested these emerging effects in a major thermal injury mouse model (3rd degree scald, ~20% TBSA) with previously documented, inflammation-mediated intestinal defects. Neutrophil extracellular traps (NETs) inflammation measurement methods were used alongside classic gut mucosa inflammation and leakiness measurements with exogenous melatonin treatment as a positive control. Our hypothesis is that simvastatin has protective therapeutic effects against early postburn gut mucosa inflammation and leakiness. To test this hypothesis, we compared untreated thermal injury (TI) adult male mice with TI littermates treated with simvastatin (0.2 mg/kg i.p., TI + SMV) immediately following burn injury and two hours before being sacrificed the day after; melatonin-treated (Mel) (1.86 mg/kg i.p., TI + Mel) mice were compared as a positive control. Mice were assessed for the following: (1) tissue oxidation and neutrophil infiltration in terminal ileum mucosa using classic carbonyl, Gr-1, and myeloperoxidase immunohistochemical or biochemical assays, (2) NETosis in terminal ileum and colon mucosa homogenates and peritoneal and fluid blood samples utilizing flow cytometric analyses of the surrogate NETosis biomarkers, picogreen and Gr-1, and (3) transepithelial gut leakiness as measured in terminal ileum and colon with FITC-dextran and transepithelial electrical resistance (TEER). Our results reveal that simvastatin and melatonin exhibit consistently comparable therapeutic protective effects against the following: (1) gut mucosa oxidative stress as revealed in the terminal ileum by markers of protein carbonylation as well as myeloperoxidase (MPO) and Gr-1 infiltration, (2) NETosis as revealed in the gut milieu, peritoneal lavage and plasma utilizing picogreen and Gr-1 flow cytometry and microscopy, and (3) transepithelial gut leakiness as assessed in the ileum and colon by FITC-dextran leakiness and TEER. Thus, simvastatin exhibits strong acute anti-inflammatory actions associated with marked decreases in gut tissue and systemic NETosis and decreased gut mucosa leakiness.

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At the end of the treatment course there was a significant elevation of HDLP2 and HDLP3 cholesterol and reduction in the levels of LDLP1-3 and LDLP cholesterol. DAS28 decreased by 0.89 points to the end of the treatment.

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* Statins reduce cholesterol concentrations and cardiovascular events in randomized clinical trials. * Much less is known about their impact in the setting of normal care.

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The purpose of this study was to formulate novel triple-layered tablet (TLT) matrices employing modified polyamide 6,10 (mPA6,10) and salted-out poly(lactic-co-glycolic acid) (s-PLGA) in an attempt to achieve stratified zero-order drug release.

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To evaluate the effects of simvastatin combined with omega-3 fatty acids on high sensitive C-reactive protein (HsCRP), lipidemia, and fibrinolysis in coronary heart disease (CHD) and CHD risk equivalent patients with mixed dyslipidemia.

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The study was aimed to assess paraoxonase-1 (PON1) activity, pleiotropic effects of simvastatin, and its relationship to Q192R and M55L polymorphisms in obese and non-obese subjects with stable coronary artery disease (CAD).

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Lipid metabolism contributes to the formation of obesity-related glomerulopathy (ORG). Heart-type fatty acid binding protein (H-FABP or FABP3) is involved in lipid metabolism and was predicted to relate to renal lesions in obesity.

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In 69 UK hospitals, 20,536 men and women aged 40-80 years at high risk of vascular events were randomly assigned to simvastatin 40 mg daily versus matching placebo for a mean of 5·0 years. Patients were categorised into six baseline CRP groups (<1·25, 1·25-1·99, 2·00-2·99, 3·00-4·99, 5·00-7·99, and ≥8·00 mg/L). The primary endpoint for subgroup analyses was major vascular events, defined as the composite of coronary death, myocardial infarction, stroke, or revascularisation. Analysis was by intention to treat. This study is registered, number ISRCTN48489393.

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Recent clinical trials recommend achieving a low-density lipoprotein cholesterol level of <100 mg/dl in high-risk and <70 mg/dl in very high risk patients. To attain these goals, however, many patients will need statins at high doses. The most frequent side effects related to the use of statins, myopathy, rhabdomyolysis, and increased levels of transaminases, are unusual. Although low and moderate doses show a favourable profile, there is concern about the tolerability of higher doses. During recent years, numerous trials to analyze the efficacy and tolerability of high doses of statins have been published. This paper updates the published data on the safety of statins at high doses.

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Statins affect the production of long chain polyunsaturated fatty acids (PUFA), both in vitro and in vivo. Various studies have shown the effects of statins on the pattern of n-6 fatty acids (FA), but limited attention has been paid to the n-3 FA. We investigated, in THP-1 and in HepG2 cells, the effects of simvastatin on the conversion of the 18C FA precursors in the n-3 and n-6 series, [1-(14)C] alpha-linolenic acid (alpha-LNA) and [1-(14)C] linoleic acid (LA) respectively, and on the metabolism of [1-(14)C] stearic acid (SA). THP-1 cells, as in the case of LA, actively converted alpha-LNA to its products, and after simvastatin treatment, the total conversion was significantly increased (from 57.2+/-7.2 to 74.3+/-8.5%, p<0.05). HepG2 cells also converted LA and alpha-LNA, but simvastatin increased significantly only the conversion of LA (9.5+/-1.9% versus 23.8+/-5.1%, p<0.02). SA conversion was similar in untreated cells (about 50%), while statin increased the production of oleic acid in HepG2, but in THP-1 cells there was a decrease. In conclusion, LA, alpha-LNA and SA are differentially metabolized in THP-1 and in HepG2 cells and their increased conversion by simvastatin is lower in HepG2 than in THP-1. These differences may reflect the distinct features of the two cell lines: monocytes, precursors of phagocytic cells, versus hepatocytes with mainly metabolic functions. Substantial differences concern also cellular FA pools: structural in THP-1 cells, and also depot, resulting in sequestering of the substrates, in HepG2. The greater n-3 FA metabolism in THP-1 cells may have favourable functional effects.

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Porcine retinal arterioles (internal diameter, 71 +/- 2 microm) were isolated and pressurized without flow for in vitro study. Diameter changes were recorded using videomicroscopic techniques. Dihydroethidium (DHE) was used to detect superoxide production.

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Clinically relevant plethoric effects associated with statin therapy in CKD patients might be restricted to the decrease of inflammation and oxidative stress.

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Self-nanoemulsifying granules were formulated with the objective of improving the bioavailability of the ezetimibe and simvastatin when administered together. Composition of self-nanoemulsifying system (SNS) was optimized using various modified oils, surfactant, and cosurfactant mixtures. SNSs were mixed with water and resultant emulsions were characterized for mean globule size and stability. SNSs were adsorbed on hydrophilic colloidal silicon dioxide to give free-flowing self-nanoemulsifying granules. Self-nanoemulsifying granules were characterized by X-ray diffraction pattern, scanning electron microscopy, dissolution profile, and for in vivo performance in hypercholesterolemic rats. X-ray diffraction studies and scanning electron microscopy indicated loss of crystallinity and/or solubilization of both drugs in the self-nanoemulsifying granules. Self-nanoemulsifying granules effected substantial increase in dissolution of the drugs as compared with pure powder of drugs. In vivo evaluation in rats showed significant decrease in the total cholesterol levels and triglyceride levels in rats as compared with positive control confirming potential of self-nanoemulsifying granules as a drug delivery system for the poorly water-soluble drugs.

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Osteoclasts, together with osteoblasts, control the amount of bone tissue and regulate bone remodeling. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. Reactive oxygen species (ROS) acts as a signal mediator in osteoclast differentiation. Simvastatin, which inhibits 3-hydroxy-3-methylglutaryl coenzyme A, is a hypolipidemic drug which is known to affect bone metabolism and suppresses osteoclastogenesis induced by receptor activator of nuclear factor-κB ligand (RANKL). In this study, we analyzed whether simvastatin can inhibit RANKL-induced osteoclastogenesis through suppression of the subsequently formed ROS and investigated whether simvastatin can inhibit H2O2-induced signaling pathways in osteoclast differentiation. We found that simvastatin decreased expression of tartrate-resistant acid phosphatase (TRAP), a genetic marker of osteoclast differentiation, and inhibited intracellular ROS generation in RAW 264.7 cell lines. ROS generation activated NF-κB, protein kinases B (AKT), mitogen-activated protein kinases signaling pathways such as c-JUN N-terminal kinases, p38 MAP kinases as well as extracellular signal- regulated kinase. Simvastatin was found to suppress these H2O2-induced signaling pathways in osteoclastogenesis. Together, these results indicate that simvastatin acts as an osteoclastogenesis inhibitor through suppression of ROS-mediated signaling pathways. This indicates that simvastatin has potential usefulness for osteoporosis and pathological bone resorption.

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Atherosclerosis was induced in rabbits by high-cholesterol feeding, and the serum was obtained from the rabbits after administration of the aqueous solution of Tongxinluo or simvastatin by gavage. U937 monocyte-derived macrophages were incubated with the sera at different concentrations for 24 hours, and the changes in MMP-9 and TIMP-1 gene expression and secretion were detected by RT-PCR and enzyme-linked immunosorbent assay, respectively.

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Epidemiological studies have shown a positive correlation between environmental particulate matter and adverse health effects. In particular, residual oil fly ash (ROFA) induces inflammation and reactive oxygen species (ROS), exerting not only local, but also systemic adverse effects. Previously, in an experimental animal model, we found that simvastatin (Sv) pretreatment was effective in preventing ROFA induced lung inflammation. Herein, using the human neuroblastoma SH-SY5Y cell line as a neurotoxicity in vitro model, we studied the potential Sv protective effect on ROFA cytotoxicity. We evaluated cell viability by the MTT assay, superoxide anion generation by NBT test, Nrf2 activation by immunofluorescence, apoptosis by cleaved-PARP and active-caspase 3 expressions, and senescence by β-galactosidase activity. SH-SY5Y cells exposed to ROFA (10 and 50μg/ml) for 24h showed decreased cell viability, increased superoxide anion generation, apoptosis and senescence. Pretreatment with Sv (1μM) for 6 days, restored cell viability to basal levels, reduced ROFA-induced O2(-) generation as well as the number of apoptotic and senescent cells. Sv pretreatment stimulated the basal and ROFA-induced levels of Nrf2 nuclear translocation suggesting that activation of the cellular antioxidant defense system prevented particle-induced oxidative stress. In parallel, rescue experiments with mevalonate did not modify the effects of SV pretreatment in any of the parameters evaluated in this study. We conclude that simvastatin may provide neuroprotection against air particulate matter-induced neurotoxicity independently of its ability to inhibit cholesterol synthesis.

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Obesity is associated with coronary artery disease. Intensive weight reducing therapy can result in improving outcome of patients after myocardial revascularization.

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It has been suggested that inflammation status, as assessed by C-reactive protein (CRP) concentration, modifies the vascular protective effects of statin therapy. In particular, there have been claims that statins might be more beneficial in people with raised CRP concentrations, and might even be ineffective in people with low concentrations of both CRP and LDL cholesterol. This study aimed to test this hypothesis.

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If severe hypotension occurs, aggressive fluid resuscitation is the first step, followed by administration of vasoactive drugs and, if necessary, by intraaortic balloon counterpulsation. If unstable angina or myocardial infarctions occurs after the use of sildenafil, the patient is treated according to the guidelines, but without nitrates.

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We noninvasively investigated 23 consecutive patients (18 men, 5 women; mean age, 56+/-7.6 years) with a mean LDL level of 165+/-34 mg/dL at baseline by PET for myocardial blood flow measurement with [13N]ammonia at rest and under dipyridamole stress (0.56 mg/kg) before and after lipid-lowering therapy with simvastatin for 6 months. Between baseline and the 6-month follow-up, total cholesterol concentration fell from 241+/-44 to 168+/-34 mg/dL, and the LDL level decreased from 165+/-34 to 95+/-26 mg/dL (P<0.001). Overall, coronary flow reserve increased from 2.2+/-0.6 to 2.64+/-0.6 (P<0.01). Maximal coronary flow increased significantly from 182+/-36 to 238+/-58 mL/minx100 g (P<0.001) at follow-up. Minimum coronary resistance declined significantly from 0. 51+/-0.12 to 0.40+/-0.14 mm Hg. mL-1. minx100 g (P<0.001). Concomitantly, a regression of anginal symptoms was observed in most patients.

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To describe the original ALS signal and to provide additional context for interpreting the signal by conducting retrospective analyses of data from long-term, placebo-controlled clinical trials of statins.

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Kruppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and thrombomodulin (TM) mRNA and protein expression were evaluated in human abdominal aortic endothelial cells (HAAEC) treated with simvastatin (0.1, 1 or 10 microM) at various levels of LSS (0, 1.25, 12.5 or 25 dynes/cm(2)).

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Statins inhibit HMG-CoA reductase, preventing synthesis of mevalonate but also of isoprenoids, which affect osteoclast activity. Amino-bisphosphonates share this effect. In vitro and in vivo, statins show convincing anabolic and anti-resorptive bone effects. However, in a clinical meta-analysis (MA), they did not prevent hip fractures.

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zocor pill cutter 2015-01-13

Almost 55% of participants reported using at least 1 medication in the past month and 14% reported using at least 5 medications. The top 5 medications reported were lisinopril, hydrochlorothiazide, simvastatin, levothyroxine, and metoprolol. Overall buy zocor prescription medication use increased significantly with age. Medication use was greater among females, former smokers, adults with body mass index (BMI) ≥ 30, or with low family income, and non-hispanic blacks. Adults having health insurance, drug coverage, or a regular source of care were more likely to report medication use.

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Statins are widely used hypocholesterolemic drugs that inhibit 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase, a rate-limiting enzyme of the mevalonate pathway whose biosynthetic endproduct is cholesterol. As a result of this activity, statins may perturb the composition of cell membranes, resulting in lipid raft disruption. Furthermore, by inhibiting protein prenylation, a process also buy zocor dependent on mevalonate, statins block membrane targeting and activity of small GTPases. Antigen uptake, processing and presentation involve the interplay of Rab and Rho family GTPases. Furthermore, lipid rafts have been implicated both in antigen internalization by the BCR and in MHC class II clustering at the immunological synapse. Here we have addressed the effects of simvastatin on antigen processing and presentation by human B cells and dendritic cells. The results show that simvastatin potently suppresses tetanus toxoid processing and presentation to CD4+ T cells by HLA-DR by inhibiting protein antigen uptake through both receptor-mediated endocytosis and macropinocytosis. This effect can be largely accounted for by defective prenylation of Rho and Rab GTPases in the absence of any measurable perturbation of lipid rafts. In addition, simvastatin was found to preferentially affect the invariant chain-dependent MHC class II pathway, thereby identifying this route of antigen processing and presentation as a selective target of statins.

zocor tablets 2017-06-27

A placebo-controlled, randomized cross-over study (three 8-week treatment periods with simvastatin (40 mg daily), bezafibrate (400 mg daily), alone and in combination) was carried out in 14 men with T2DM. Cholesterol efflux was determined using human THP-1 monocyte-derived macrophages, HDL antioxidative capacity was buy zocor measured as inhibition of low-density lipoprotein oxidation in vitro, and HDL anti-inflammatory capacity was assessed as suppression of thrombin-induced monocyte chemotactic protein 1 expression in human umbilical vein endothelial cells. Pre-β-HDL was assayed using crossed immunoelectrophoresis.

zocor generic name 2017-03-30

Pneumonectomized rats injected with monocrotaline at 4 weeks demonstrated severe PAH at 11 weeks (mean pulmonary artery pressure [mPAP]=42 versus 17 mm Hg in normal rats) and death by 15 weeks. When rats with severe PAH received simvastatin (2 mg x kg(-1) x d(-1) by gavage) from week 11, there was 100% survival and reversal of PAH after 2 weeks (mPAP=36 mm Hg) and 6 weeks (mPAP=24 mm Hg) of therapy. Simvastatin treatment reduced right ventricular hypertrophy and reduced proliferation and increased apoptosis of pathological smooth muscle cells in the neointima and medial walls of pulmonary arteries. Longitudinal transcriptional profiling buy zocor revealed that simvastatin downregulated the inflammatory genes fos, jun, and tumor necrosis factor-alpha and upregulated the cell cycle inhibitor p27Kip1, endothelial nitric oxide synthase, and bone morphogenetic protein receptor type 1a.

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To support drug development, the drug-drug interaction potential (DDI) of an investigational drug (AZX) was assessed against the probe estradiol 17β-glucuronide as well as against simvastatin acid, atorvastatin, pravastatin, pitavastatin, fluvastatin, rosuvastatin and estrone 3-sulfate. The inhibitory potentials of the OATP1B1 inhibitors rifamycin SV and gemfibrozil were assessed in parallel. Monolayer cellular uptake assays were used to determine inhibition of human OATP1B1. Apparent K(m) values for the OATP1B1-mediated transport of [(3) buy zocor H] substrates were determined prior to their use as probes in inhibition studies, and ranged from 0.6 to 29 μM for statins. The K(m) of lipophilic simvastatin acid could not be determined due to its high passive permeability that masked OATP1B1 transport, and therefore this statin could not be used as a probe. Estrone 3-sulfate exhibited biphasic kinetics, whereas estradiol 17β-glucuronide demonstrated simple Michaelis-Menton kinetics. AZX moderately inhibited OATP1B1-mediated transport of all statins (IC(50)=4.6-9.7 μM), except fluvastatin, of estradiol 17β-glucuronide (IC(50)=5.3 μM), and weakly inhibited estrone 3-sulfate (IC(50)=79 μM). Rifamycin SV strongly, and gemfibrozil weakly, inhibited the OATP1B1-mediated transport of substrates. Estradiol 17β-glucuronide was identified as a good surrogate probe for statins when assessing OATP1B1 inhibitory potential using this test system. Inhibition data was used to predict the likelihood of a clinical DDI, using current draft US FDA guidance and recommendations of the International Transporter Consortium. Predictions for AZX indicated the potential for an OATP1B1-mediated DDI in vivo and that a clinical interaction study is warranted to confirm whether AZX is an OATP1B1 inhibitor in the clinic.

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To determine the effect of switching drugs on the compliance and persistence of new statin buy zocor users.

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We tested the hypothesis that, compared with placebo, simvastatin would reduce the progression of coronary artery calcium (CAC) and abdominal aortic calcium (AAC) levels in participants asymptomatic for vascular disease. Total CAC and AAC were measured with multidetector cardiac computed tomography. Inclusion criteria were a CAC score of >or=50 Agatston units, high-density lipoprotein (HDL) cholesterol levelbuy zocor /dl, and >or=2 other risk factors. Diabetes and history of vascular disease were exclusion criteria. Participants were randomized to receive 80 mg simvastatin (n=40) or matching placebo (n=40) for 12 months. Lipids were measured at 3-month intervals, and CAC and AAC measurements were repeated at 6 and 12 months. Total cholesterol, triglycerides, and LDL decreased significantly with simvastatin treatment (p<0.0001 for all comparisons, adjusted for baseline levels), whereas lipids remained unchanged for subjects randomized to receive placebo. Total CAC volume increased from baseline in both treatment groups. For subjects in the active treatment group, CAC volume increased by 9%, whereas in the placebo group, plaque volume increased by 5% (p=0.12 for treatment effect). AAC volume also increased in both treatment groups (p=0.15 for treatment effect). In conclusion, simvastatin treatment does not reduce progression of CAC or AAC compared with placebo.

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Among T2DM subjects, simvastatin lowered TC and LDL-C from the baseline (-25±4% and -40±5%, respectively, P<0.001), whereas ezetimibe was not as effective (-2±4% and -3±5%, respectively). Among buy zocor T1DM subjects, both statin and ezetimibe showed significant decreases in TC and LDL-C from baseline, although ezetimibe lowered LDL-C much more than simvastatin (-32±12 (P<0.001) and -19±5% (P<0.01), respectively). Effect of simvastatin on LDL-C was much lower among T1DM subjects compared to T2DM subjects (P=0.02).

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The scaffold porosity was more than 90% with an average aperture of 200-300 μm. The drug released slowly. There was no obvious interpretation. Type I collagen showed positive expression. Alizarin red staining proofed the formation of mineralization nodules in group which was induced with the conditional medium and simvastatin. 0.5 mg group showed buy zocor cells adhered to the inner surface of the scaffold material and could significantly promote the proliferation and differentiation of cells.

zocor recommended dosage 2016-11-01

A case-control design was used to compare C-reactive protein (CRP buy zocor ) levels, seropositivity for Chlamydia pneumoniae and Helicobacter pylori, and anti-oxidized low-density lipoprotein (oxLDL) antibody levels in prerandomization blood samples from 129 participants in the Scandinavian Simvastatin Survival Study who died (cases), and from 129 matched participants who were alive during 5-year follow-up (controls).

zocor dosage forms 2015-06-08

The effect of 24 weeks of treatment with simvastatin, a new HMG coenzyme A reductase inhibitor (dosages of 20 and 40 mg day-1) on serum lipid, lipoprotein and apolipoprotein A-I and B concentrations as well as safety parameters and subjective side effects were studied in 11 patients with familial (FH) and 10 patients with polygenic hypercholesterolaemia (P-HC). The effects on plasma lipoprotein and apolipoprotein concentrations had already been achieved after four weeks in both groups and then remained during the study. In FH, mean fasting plasma total cholesterol concentration decreased from 10.51 to 6.71 mmol l-1 (36%), and in P-HC from 6.55 to 4.54 mmol l-1 (31%) at 24 weeks (P less than 0.001). Mean plasma low density lipoprotein (LDL) cholesterol concentrations also decreased, in FH from 8.87 to 5.05 mmol l-1 (43%) and in P-HC from 4.97 to 3.12 mmol l-1 (37%) at 24 weeks (P less than 0.001). Furthermore, apolipoprotein B concentrations decreased significantly from 2.21 to 1.57 g l-1 (29%) (less than 0.001) in FH and from 1 buy zocor .53 to 1.09 g l-1 (29%) (P less than 0.01) in P-HC. Plasma high density lipoprotein (HDL) cholesterol increased in both FH and P-HC during treatment. Increases were seen in both the subfractions HDL2 and HDL3. Simvastatin was well tolerated. No serious clinical or laboratory adverse effects were observed. It is concluded that 24 weeks of treatment with simvastatin in doses up to 40 mg day-1 effectively reduces plasma total and LDL cholesterol concentrations without causing subjective or significant objective side effects. Thus, simvastatin may be of great interest in future studies for prevention of coronary heart disease due to hypercholesterolaemia.

simvastatin zocor generic 2016-11-17

The sickle cell disease (SCD) is a hemolytic genetic anemia characterized by free heme and hemoglobin release into intravascular spaces, with endothelial activation. Heme is a proinflammatory molecule able to directly activate vascular endothelium, thus, endothelial dysfunction and vascular disease are major buy zocor chronic events described in SCD. The aim of this study was to evaluate the production of endothelial nitric oxide synthase (eNOS), nitrite and hypoxia inducible factor alpha (HIF-α) in HUVECs (human umbilical vein endothelial cells) activated by heme in response to simvastatin, hydroxyurea (HU), and ascorbic acid therapies. eNOS and HIF-α production were evaluated by ELISA and nitrite was measured by the Griess technique. The production of HIF-α increased when the cells were stimulated by heme (p<0.01), while treatment with HU and simvastatin reduced the production (p<0.01), and treatment with ascorbic acid increased HIF-1a production by the cells (p<0.01). Heme increased eNOS production, (p<0.01) but showed a heterogeneous pattern, and the lowest concentrations of all the treatments reduced the enzyme production (p<0.01). The nitrite production by HUVECs was enhanced by stimulation with heme (p<0.001) and was reduced by treatment with HU (p<0.001), ascorbic acid (p<0.001) and simvastatin (p<0.01). In summary, our results suggest that the hemolytic vascular microenvironment in SCD requires different therapeutic approaches to promote clinical improvement, and that a combination of therapies may be a viable strategy for treating patients.

zocor overdose 2016-04-09

Since statins and angiotensin receptor blockers are a frequently prescribed combination in patients with atherosclerotic cardiovascular buy zocor diseases, we tested the interactive effects of simvastatin and losartan on atherosclerosis in apolipoprotein E (apoE)(-/-) mice.

zocor 500 mg 2017-07-24

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system and is considered to be caused by the binding of NMO-IgG to aquaporin 4 (AQP4) on astrocytes, which initiates complement-dependent cytotoxicity. AQP4 has two isoforms, i.e., M1 and M23. AQP4 is considered to form heterotetramers containing both isoforms in vivo. Most of the previous studies were performed using either one of the isoforms expressing cell lines. In this study, we generated a fluorescent epitope-tagged AQP4 M1 and M23 co-expressing astrocyte cell line and examined the subcellular targeting of AQP4. In this cell line, AQP4 was targeted mostly to membrane lipid rafts fraction evidenced by sucrose density gradient ultracentrifugation followed by Western blotting with anti-AQP4 antibody. Cholesterol depletion with methyl-β-cyclodextrin or simvastatin resulted in the dislocation (relocation) of AQP4 from lipid rafts to non-rafts fraction of the membrane and AQP4 was not internalized intracellularly. This change in the localization of AQP4 on membrane significantly reduced complement-dependent cytotoxic effects of NMO-IgG obtained from patients with NMO without affecting AQP4 orthogonal arrays. Thus, these data strongly suggest that the targeting buy zocor of AQP4 in the lipid rafts is closely related to the pathogenic effects of NMO-IgG.

zocor and alcohol 2015-06-07

ADAMTS13 is a specific von Willebrand factor-cleaving protease. Severe deficiency of ADAMTS13 is the main cause of thrombotic Cozaar Normal Dosage thrombocytopenic purpura. ADAMTS13 is mainly synthesized and released from hepatic stellate cells and endothelial cells, but is also expressed in other cells, including kidney podocytes. Simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has a beneficial effect on atherosclerosis and also has anti-inflammatory and antithrombotic properties. A recent study indicates that ADAMTS13 reduces inflammatory plaque formation during early atherosclerosis in mice. In our study, we investigated the effects of simvastatin on inflammatory cytokines-induced ADAMTS13 expression in podocytes.

zocor maximum dosage 2015-07-10

Simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has antioxidant and anti-inflammatory Cymbalta Buy properties that are independent of lipid-lowering abilities. This experiment was carried out to explore the effects of simvastatin on apoptosis in vulnerable atherosclerotic plaques of apoE-deficient mice.

zocor 50 mg 2016-08-16

Over a mean of 10.5 years of follow-up, we identified 11,555 NMSC cases. Compared with participants with no statin use, use of any statin at baseline was associated with significantly increased NMSC incidence (adjusted odds ratio (ORadj) 1.21; 95% confidence interval (CI): 1. Avelox Alcohol 07-1.35)). In particular, lovastatin (OR 1.52; 95% CI: 1.08-2.16), simvastatin (OR 1.38; 95% CI: 1.12-1.69), and lipophilic statins (OR 1.39; 95% CI: 1.18-1.64) were associated with higher NMSC risk. Low and high, but not medium, potency statins were associated with higher NMSC risk. No significant effect modification of the statin-NMSC relationship was found for age, BMI, smoking, solar irradiation, vitamin D use, and skin cancer history.

zocor tab 10mg 2016-04-12

Surgery for morbid obesity is rapidly increasing. Patients undergoing bariatric surgery are prone to gallstone development during the rapid weight loss. These patients are often given medications such as ursodeoxycholic acid to prevent gallstone formation; however, these medications are often poorly Betnovate Generic tolerated by patients, who subsequently discontinue them. We performed a study in a lithogenic animal model to assess the effectiveness of a potential alternate medication for gallstone prevention.

zocor 20 mg 2016-10-20

The benefit of statins in patients with acute aneurysmal subarachnoid haemorrhage is unclear. We aimed to determine whether simvastatin 40 mg could improve the long-term outcome Geodon Overdose Emedicine in patients with this disorder.

zocor 40mg tab 2017-08-13

In Czech Tegretol Syrup 300ml patients treated with low statin doses, there is no association between SLCO1B1 gene polymorphism and risk of myalgia/myopathy.

zocor oval pill 2015-08-23

For measurements of cholesterol and fatty acid synthesis rates, human lenses were incubated for 20 hr in the presence of [14C]-acetate, and pravastatin or simvastatin. Radiolabeled [14C]-cholesterol and [14C]-fatty acids were determined. To avoid the influence of individual differences, one lens from each donor was incubated without drug (control) and the other lens was incubated in the presence of drug. For each lens pair, the percentage inhibition of the cholesterol synthesis caused by the drug was calculated. Fatty acid synthesis was not influenced by the drugs. By comparing the fatty acid synthesis rate of the drug-incubated with the control lens of a pair, a predefined exclusion criterion was used to eliminate lens pairs in which the lenses had no comparable biosynthetic capacities.

zocor 60 mg 2016-11-26

These findings report for the first time that cyclin D1 expression is deregulated in IPF through a RhoA dependent mechanism that influences lung fibroblast proliferation. This potentially unravels new molecular targets for future anti-IPF strategies; accordingly, Simvastatin inhibition of Rho-mediated cyclin D1 expression in IPF fibroblasts merits further exploitation.

zocor generic brand 2016-12-30

The results indicated that probiotic microorganism E. faecium CRL 183 could be used to improve the lipid profile as an alternative or an adjuvant for drug therapy. The effectiveness of simvastatin in the management of blood lipid was confirmed. There were no effects of soy isoflavones, E. faecium and simvastatin on atherosclerosis development.