جستجوی مقالات مرتبط با کلیدواژه « Rosuvastatin » در نشریات گروه « پزشکی »

Rosuvastatin (RSV) is a hydrophilic, effective statin with a long half-life that stimulates bone regeneration. The present study aims to develop a new scaffold and controlled release system for RSV with favourable properties for bone tissue engineering (BTE).

In this experimental study, high porous polycaprolactone (PCL)-gelatin scaffolds that contained different concentrations of RSV (0 mg/10 ml, 0.1 mg/10 ml, 0.5 mg/10 ml, 2.5 mg/10 ml, 12.5 mg/10 ml, and 62.5 mg/10 ml) were fabricated by the thermally-induced phase separation (TIPS) method. Mechanical and biological properties of the scaffolds were evaluated by Fourier transform infrared spectroscopy (FTIR), scanning electron microscope (SEM), compressive strength, porosity, MTT, alkaline phosphatase (ALP) activity, water contact angle, degradation rate, pH alteration, blood clotting index (BCI), and hemocompatibility.

SEM analysis confirmed that the porous structure of the scaffolds contained interconnected pores. FTIR results showed that the RSV structure was maintained during the scaffold's fabrication. RSV (up to 62.5 mg/10 ml) increased compressive strength (16.342 ± 1.79 MPa), wettability (70.2), and degradation rate of the scaffolds. Scaffolds that contained 2.5 mg/10 ml RSV had the best effect on the human umbilical cord mesenchymal stem cell (HUC-MSCs) survival, hemocompatibility, and BCI. As a sustained release system, only 31.68 ± 0.1% of RSV was released from the PCL-Gelatin-2.5 mg/10 ml RSV scaffold over 30 days. In addition, the results of ALP activity showed that RSV increased the osteogenic differentiation potential of the scaffolds.

PCL-Gelatin-2.5 mg/10 ml RSV scaffolds have favorable mechanical, physical, and osteogenic properties for bone tissue and provide a favorable release system for RSV. They can mentioned as a a promising strategy for bone regeneration that should be further assessed in animals and clinical studies.

 Vascular stenosis is one of the causes of cardiovascular diseases (CVDs). Implementing appropriate therapeutic measures for CVDs requires preventing the progression of stenosis. The purpose of this study was to evaluate the efficacy of atorvastatin and rosuvastatin on the levels of alpha and beta apolipoproteins using systematic review and meta-analysis.

 This review was performed based on the PRISMA protocol. The ISI, Cochrane Library, Google Scholar, PubMed, and Scopus databases were independently searched by two researchers. MeSH keywords were used to recruit related articles published between 2005 and 2018. Meta-analysis was conducted in STATA 11.1software.

 A total of 65 articles were found. Out of these, nine studies were ultimately included in meta-analysis. The findings showed that alpha lipoprotein level increased by 4.24 mg/dl (95% CI: -0.03; -8.45) and 8.71 mg/dl (95% CI: -1.95; -15.48) in patients treated with atorvastatin and rosuvastatin, respectively. Also, patients treated with either atorvastatin or rosuvastatin showed 40.55mg/dl (95% CI: 32.16; 45.93) and 44.78 g/dl (95% CI: 34.16; 55.39) decreases in beta-lipoprotein levels, respectively.

 According to the results, rosuvastatin is more effective than atorvastatin in reducing alpha apolipoprotein and increasing beta apolipoprotein levels within a short period of time.

As a promising revascularization therapy, percutaneous coronary intervention (PCI) is widely used in patients with coronary artery disease. No-reflow and low thrombolysis in myocardial infarction (TIMI) flow are two adverse periprocedural events.

This study aimed to compare the effectiveness of atorvastatin and rosuvastatin in reducing the no-reflow phenomenon in patients undergoing primary PCI.

Following a randomized control design, 280 eligible patients with no history of MI or ischemic heart disease (IHD) with ST-elevation myocardial infarction (STEMI) who were candidates for coronary angioplasty underwent angioplasty from May 2020 to December 2020.

Our results showed that TIMI flow III was significantly higher in the rosuvastatin group, while the no-reflow was not seen in this group (P < 0.001). Also, ST resolution after 90 minutes of PCI was significantly better in the rosuvastatin group.

This study demonstrated that using a loading dose of rosuvastatin could reduce the no-reflow phenomenon in patients undergoing primary PCI.

Rosuvastatin is the newest statin family drug and acts as an HMG-CoA reductase inhibitor. Rosuvastatin can decrease the amount of cholesterol made by the liver and reduce the risk of heart disease. Since liver diseases are one of the significant causes of morbidity and mortality due to drugs toxicity, it is essential to check the liver’s function during widely used drugs such as rosuvastatin. Therefore, this study aimed to investigate the effect of rosuvastatin on the liver in the mature female NMRI mouse strain.

In this experimental study, 30 adult female NMRI strains (mice) at a mean weight of 25-30 grams were divided into five groups control, sham, and treatment groups. The mice of treated groups, including 1, 2, and 3, received rosuvastatin in doses of 10, 20, and 40 mg/Kg of body mass by oral gavage for 21 days. The mice in all groups were dissected after completing the gavage, their hearts were examined, and blood samples were obtained to measure liver enzymes. Then, the mice were sacrificed, and the liver tissue was subjected to antioxidant enzymes. The ELISA test measured the concentrations of the antioxidant and liver enzymes.

The results showed that rosuvastatin decreased GPX, MDA, and FRAP with an increase in SOD, AST, and ALT (P<0.05).

It was concluded that high doses of rosuvastatin could damage the liver.

Statins are the most common drugs used for reducing low-density lipids (LDL). In addition to their lipid-lowering effects, they have well-documented anti-inflammatory actions. The goal of this study was to compare the effects of high dose atorvastatin and rosuvastatin on lipid profiles and high sensitivity C Reactive Protein (hs-CRP) in patients undergoing percutaneous coronary intervention (PCI).

The study was done between October 2017 and September 2018 in Semnan Kowsar Hospital. In this randomized trial, 69 patients with atherosclerotic coronary artery disease were randomly assigned 1:1 to receive atorvastatin (80 mg daily) or rosuvastatin (40 mg daily) for 4 months. Levels of hs-CRP and lipid profiles including cholesterol, triglyceride, low-density lipids (LDL), and high-density lipids (HDL) were measured and compared before and after the treatments. Lipid profiles were measured at baseline, 2 months, and 4 months of the treatment.

Sixty patients completed the study. The mean age was 61.1 ± 6.6 years with an excess of males. After 4 months, both drugs could significantly reduce LDL levels, however, the between- group differences were not statistically significant. Rosuvastatin significantly increased HDL levels (p < 0.05). In addition, triglyceride levels had a significant reduction in both groups, yet the differences were not significant. Both drugs caused significant reductions in hs-CRP levels (p < 0.05). Moreover, the effects of treatments were seen in drug naïve patients as well as patients who were on statins prior to the trial.

The results indicate that high dose therapies with atorvastatin and rosuvastatin have similar effects on lipid profiles and hs-CRP levels in patients undergoing PCI.

Considering the cardioprotective and anti-inflammatory properties of statins, the aim of the present experiment was to investigate the possible involvement of inflammatory cytokines in anti-arrhythmic effects of rosuvastatin in both in vitro and in vivo experiments in rats.

Three weeks after oral administration of either of rosuvastatin or vehicle, the atria were removed and after incubation with ouabain, time of onset of arrhythmia and asystole were recorded. We also used immunohistochemistry technique to identify the differentially expressed proteins interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α in atria.

Rosuvastatin significantly postponed the onset of arrhythmia compared to vehicle-treated group. Injection of ouabain increased the atrial expression of IL-1β, IL-6 and TNF-α proteins, while pretreatment of rats with rosuvastatin could significantly attenuate them.

Our data suggest that rosuvastatin exerts anti-arrhythmic properties at least in part through modulation of inflammatory cytokines.

Bone regeneration can be accelerated by localized delivery of statins. Here, we aimed to evaluate the effect of two thermosensitive hydrogels containing rosuvastatin (RSV) on proliferation and differentiation of human osteoblast-like MG-63 cells.
Experimental approach: Firstly, chitosan (CTS)/glycerophosphate (GP)/gelatin (G) thermosensitive hydrogel was prepared and characterized based on rheological properties, in vitro erosion, and release pattern of RSV and then the optimized mixture was loaded with nanoparticles containing RSV(NRSV).  Secondly, the effect of NRSV-embedded in CTS/GP/G on cell viability, alkaline phosphate activity,  and cell calcification was evaluated using MG-63 cells and compared with RSV-embedded into hyaluronic acid (HA)/Pluronic® F127 (PF127) hydrogel. 

CTS/GP mixtures with 1 and 1.5 % gelatin existing in solution with low viscosity at  4 °C were solidified at 32-34 °C while the mixture containing 2% gelatin was jellified at room temperature. The gelation times of CTS/GP/G with 1 and 1.5% gelatin were 72 and 44 s, respectively. The hydrogel containing 3% w/v NRSV was also converted to a semisolid upon increasing the temperature to 33-36 °C. Due to the higher gel strength of CTS/GP/G compared to HA/PF127 hydrogel, the release rate of RSV from the NRSV-embedded CTS/GP/G hydrogel was significantly slower than that of HA/PF127 system. As revealed by alkaline phosphatase and mineralization assays, NRSV-embedded in CTS/GP/G hydrogel had the most promotive effect on differentiation of osteoblasts among other mixtures.

NRSV-embedded in CTS/GP/G hydrogel could be efficiently used in the future for bone defects such as osteoporosis and bone fractures.

The most reported form of statin induced pain is myalgia, conversely peripheral neuropathy is a rare side effect. We report a patient who received rosuvastatin for hypercholesterolemia and experienced episodes of pain in both hands during the night. Rosuvastatin was stopped and atorvastatin was replaced. Re-introduction with another statin resulted in a more severe form of the similar adverse effect after 4 months. This is a rare adverse effect of a extensively prescribed class of drug. Physicians should be aware of the possibility of peripheral neuropathy symptoms in patients on statin therapy.

Hypercholesterolemia is a common metabolic disorder in developing and developed countries and is associated with the increased rates of chronic kidney disease (CKD). Statin therapy could reduce cholesterol synthesis as well as progression of CKD. Diversity between statins causes variety in pharmacokinetics and pharmacodynamics and also their pleiotropic effects. In the present investigation we aimed to evaluate the protective potentials of both atorvastatin (Ator) (as lipid-soluble statin) and rosuvastatin (Ros) (as water-soluble statin) against renal histopathological damages in the high cholesterol diet induced hypercholesterolemic rats (HCDIHR).

Serum lipid profile, oxidized low density lipoprotein (OX-LDL), malondialdehyde (MDA), urea and creatinine levels, as well as renal histopathology were evaluated.

While Ros acted better than Ator to reduce serum low density lipoprotein cholesterol (LDL-C) (P<0.01), atherogenic index (AI) (P<0.01), MDA (P<0.01), and OX-LDL (P<0.01); no significant differences were noted in their cholesterol (P=0.72), triglyceride (TG) (P=0.79), and very low density lipoprotein cholesterol lowering (VLDL-C) (P=0.79) and high density lipoprotein cholesterol elevating effects (HDL-C) (P=0.72). Ator was more effective to reduce renal histopathologic indices compared to Ros, including accumulation of lipid droplet, glomerular foam cells, mesangial cell proliferation, renal hemorrhage, and tubulointerstitial damages in the kidneys of diet induced hypercholesterolemic rats.

The findings underline that the lipophilic Ator may performs better than Ros in attenuating renal damages in HCDIHR.

Statins provide greater protection than predicted from just cholesterol-lowering effects, which is possibly mediated by other pleiotropic actions. This study aimed to examine the possible interaction effect of asthma on lipid profiles and evaluate the effect of rosuvastatin treatment on asthma. The animals were assigned into (1) control, (2) asthmatic, (3) hyperlipidemic, (4) asthmatic-hyperlipidemic, (5) rosuvastatin (40 mg/kg/day intraperitoneally, for 3 weeks)-treated asthmatic, (6) rosuvastatin-treated hyperlipidemic and (7) rosuvastatin-treated asthmatic-hyperlipidemic groups. Tracheal responsiveness to methacholine and ovalbumin, total and differential WBC (white blood cell) counts, and oxidative stress markers in bronchoalveolar lavage fluid (BALF) were evaluated. In the asthmatic and asthmatic-hyperlipidemic groups, tracheal responsiveness to ovalbumin, total WBC count, numbers of eosinophils, neutrophils, and monocytes were higher than the control group (p<0.001). A left-ward shift in the concentration-response curves to methacholine, an increase in nitrite and malondialdehyde concentrations, and a decrease in total thiol content, superoxide dismutase and catalase activities were also observed in the asthmatic and asthmatic-hyperlipidemic groups compared to control group (p<0.01 to p<0.001). Beyond lipid-lowering effect in the treated hyperlipidemic and asthmatic-hyperlipidemic groups, rosuvastatin treatment decreased tracheal responsiveness to methacholine, reduced total WBC count, the numbers of eosinophils, neutrophils, and monocytes, as well as decreased malondialdehyde concentration, and increased total thiol content, superoxide dismutase and catalase activities in treated asthmatic and asthmatic-hyperlipidemic groups (p<0.05 to p<0.001). The improving effect of rosuvastatin on asthmatic and asthmatic-hyperlipidemic animals was shown due to pleiotropic mechanisms including the effect on airway hyperresponsiveness, lung inflammation, and oxidative stress.