Influence Of Rosuvastatin Research Articles

Influence of rosuvastatin on apolipoproteins and coagulation factor levels: Results from the STAtin Reduce Thrombophilia trial

BackgroundThe STAtins Reduce Thrombophilia trial showed that, in patients with prior venous thrombosis, rosuvastatin decreased various coagulation factor levels. ObjectivesHere, we investigated the hypothesis that statins decrease coagulation factor levels through shared mechanisms of synthesis or regulatory pathways with apolipoproteins. MethodsWe measured the levels of apolipoprotein (Apo)A-I, A-II, A-IV, (a), B-100, B-total, C-I, C-II, C-III, and E in patients (n = 126) randomized to 28 days of rosuvastatin use. We assessed the association between apolipoproteins and coagulation factors at baseline using linear regression. The mean difference in apolipoprotein levels between baseline and after 28 days of rosuvastatin use was determined through linear regression, adjusting for age, sex, and body mass index. Coagulation factors were added to this model to determine if the lowering of apolipoproteins by rosuvastatin was linked with coagulation factor levels. ResultsAt baseline, levels of all apolipoproteins, except Apo(a), were positively associated with FVII, FIX, and FXI. Apolipoproteins levels, except for ApoA-I, A-IV, and Apo(a), were decreased after 28 days of rosuvastatin. ApoB-100 showed the largest mean decrease of -0.43 g/L (95% CI = −0.46 to −0.40). The decrease in ApoC-I and C-III levels was associated with a decrease in FVII, whereas the decrease in apoA-II, B-100, and B-total was associated with a decrease in FXI. The decrease in apolipoproteins was neither associated with FVIII or vWF decrease nor with endogenous thrombin potential changes. ConclusionsRosuvastatin decreases the level of several apolipoproteins, but this decrease was associated only with a decrease in FVII and XI and not with FVIII/vWF.

The influence of rosuvastatin on the efficacy of standard triple eradication therapy in patients with gallstone disease and Helicobacter pylori infection

The influence of rosuvastatin on the efficacy of standard triple eradication therapy in patients with gallstone disease and Helicobacter pylori infection

Ameliorative Potential of Rosuvastatin on Doxorubicin-induced Cardiotoxicity by Modulating Oxidative Damage in Rats

The study aimed to explore the in vivo protective potential of rosuvastatin (ROSS), an oral antihyperlipidemic drug against doxorubicin (DOXO) induced cardio toxicity in rats. Cardiac toxicity was induced by DOXO injection (10 mg/kg, i.p.), once on the 20th day of the experiment. Except for the control rats, all were received DOXO and the study was continued for up to 21 days. The influence of ROSS on acute treatment was analyzed by quantification of cardiac marker enzymes such as creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) and liver marker enzymes like aspartate aminotransferase (AST), alanine aminotransferase (ALT) along with the measurement of in vivo antioxidants like superoxide dismutase and catalase. To observe histological changes of myocardial tissue hematoxylin and eosin staining were used. Acute administration of DOXO resulted in a marked rise of cardiac marker enzymes that confirms the myocardial damage compared to control animals whereas administration of ROSS (10 mg/kg, p.o.) resulted in the significant reduction of CK-MB, LDH levels (p<0.05) and AST, ALT levels to a remarkable extent. Moreover, ROSS administration significantly increased the activities of various in vivo antioxidant levels. From the results, the acute administration of ROSS showed significant cardioprotective property, which was evidenced by a significant reduction of cardiac and liver marker enzymes along with significant improvement of in vivo antioxidant activities. Furthermore the results were supported with histopathological observations. Hence, it can be concluded that cardioprotective potential of ROSS may be through attenuation of oxidative stress by modulating oxidative damage in rats.

Influence of rosuvastatin combined with noninvasive positive pressure ventilation on pulmonary ventilation function, SGRQ score and laboratory parameters of patients with AECOPD

Objective To investigate the influence of rosuvastatin combined with noninvasive positive pressure ventilation on pulmonary ventilation function, SGRQ score and laboratory parameters of patients with AECOPD. Methods 110 patients with AECOPD were chosen and they were randomly divided into two groups according to the digital table, each group in 55cases.The control group received noninvasive positive pressure ventilation, and the observation group received rosuvastatin on the basis of the control group.The number of acute exacerbation and re-hospitalization, pulmonary ventilation function, SGRQ score, 6MWT, the levels of IL-8, CRP, alanine aminotransferase, triacylglycerol and total cholesterol before and after treatment of the two groups were compared. Results The number of acute exacerbation and re-hospitalization of the observation group were significantly lower than those of the control group(t=3.19, 2.84, all P<0.05). The levels of FEV1 and FEV1/FVC after treatment of both two groups were significantly higher than before treatment(t=2.88, 3.14, 2.90, 3.42, all P<0.05). The levels of FEV1 and FEV1/ FVC after treatment of the observation group were significantly higher than those of the control group(t=2.38, 2.61, all P<0.05). The SGRQ scores and 6MWT after treatment of both two groups were significantly better than those before treatment(t=2.59, 2.51, 2.84, 3.17, all P<0.05). The SGRQ scores and 6MWT after treatment of observation group were significantly better than those of the control group (t=2.59, 2.51, all P<0.05). The levels of the IL-8, CRP, alanine aminotransferase, triacylglycerol and total cholesterol after treatment of both two groups were significantly lower than those before treatment (t=2.78, 2.50, 2.94, 3.07, 4.26, 3.89, 3.02.3.67, all P<0.05). The levels of IL-8, CRP, alanine aminotransferase, triacylglycerol and total cholesterol after treatment of the observation group were significantly lower than those of the control group(t=2.64, 2.33, 2.81, 3.15, all P<0.05). Conclusion Rosuvastatin combined with noninvasive positive pressure ventilation in the treatment of patients with AECOPD can efficiently promote lung function recovery, higher quality of life and exercise endurance, improve the laboratory indicators and is help to avoid the acute attack and re-hospitalization for long-term. Key words: Pulmonary disease, chronic obstructive; Intermittent positive-pressure ventilation; Rosuvastatin

Influence of rosuvastatin on inflammatory factors and immune function in chronic obstructive pulmonary disease with pulmonary heart disease

Objective To investigate the influence of rosuvastatin on inflammatory factors and immune function in chronic obstructive pulmonary disease(COPD) with pulmonary heart disease. Methods 80 COPD patients with pulmonary heart disease were randomly divided into two groups, 40 cases in each group.The control group was treated with conventional medicine comprehensive treatment, the observation group was given rosuvastatin based on the control group.The inflammatory cytokines (TNF-α, IL-1 and hs-CRP) changes, immunoglobulin IgM, IgG and IgA changes situation, and heart, lung function changes related indicators were compared between the two groups before and after the treatment. Results After treatment, the TNF-α, IL-1 and hs CRP levels of the observation group were significantly lower than those before treatment(t=145.5, 35.35, 57.5, all P<0.05) and those of the control group(t=160.75, 11.45, 32.99, all P<0.05). After treatment, the IgM, IgG and IgA levels of the observation group were significantly lower than those before treatment (t=4.89 of 18.29, 3.42, all P<0.05) and those of the control group (t=2.55 9.67, 2.342, all P<0.05). After treatment, the FEV1, FEV1/FVC and LVEF of the observation group were significantly higher than those before treatment(t=40.44 33.64, 33.79, all P<0.05), while the PAP level was significantly lower than that before treatment (t=24.12, P<0.05), and the FEV1, FEV1/FVC and LVEF of the observation group were significantly higher than those of the control group after treatment(t=16.30, 15.82, 18.72, all P<0.05), while the PAP level was significantly lower than that of the control group after treatment(t=13.43, P<0.05). Conclusion Combined rosuvastatin therapy for COPD patients with pulmonary heart disease can effectively reduce body inflammatory response, improve immune function and myocardial contractility, so it can promote functional recovery of heart and lung in patients. Key words: Rosuvastatin; Pulmonary heart disease; Pulmonary disease, chronic obstructive; Inflammatory factors; Immune function

Influence of Rosuvastatin on Blood Lipids, Inflammatory Factors, Oxidative Stress and Matrix Metalloproteinases in Patients with Chronic Heart Failure

Influence of Rosuvastatin on Blood Lipids, Inflammatory Factors, Oxidative Stress and Matrix Metalloproteinases in Patients with Chronic Heart Failure

Rosuvastatin reduces platelet recruitment by inhibiting NADPH oxidase activation

Rosuvastatin increased vascular endothelial NO and attenuated platelet activation after ischemia-reperfusion in mice; nevertheless, the influence of rosuvastatin on the activation of human platelets and the underlying mechanism has never been investigated.In an in vitro study platelets from 8 healthy donors were incubated with scalar concentrations of rosuvastatin (1–10μM) before activation. Platelet recruitment (PR), that mimics the propagation of platelet aggregation and is dependent upon isoprostane formation, was investigated. PR was inhibited by rosuvastatin in concentration-dependent manner concomitantly with down-regulation of platelet release of the pro-thrombotic molecule CD40L. This effect was associated with lower production of platelet reactive oxygen species (ROS), isoprostane and activation of the glycoprotein IIb/IIIa and was counteracted by exogenous addition of isoprostanes. Conversely, rosuvastatin concentration-dependently increased platelet NO. Platelet isoprostane formation mainly depends from NADPH oxidase. Rosuvastatin concentration-dependently inhibited platelet sNOX2-dp release, a specific marker of NADPH oxidase activation, PKC phosphorylation and p47phox translocation from cytosol to membranes.In an ex vivo study 10 hypercolesterolemic patients were randomly allocated to diet or rosuvastatin (20mg). We observed that as early as 2h after rosuvastatin PR, platelet isoprostanes formation, platelet CD40L and sNOX2-dp decreased while platelet NO increased; no changes were detected in diet-assigned patients.This study shows that in vitro rosuvastatin impairs platelet activation via inhibition of NOX2-derived oxidative stress. This effect, which is associated ex vivo with acute inhibition of platelet activation, suggests that rosuvastatin behaves as an antiplatelet drug.

Influence of rosuvastatin on the NAD(P)H oxidase activity in the retina and electroretinographic response of spontaneously hypertensive rats

Retinal complications may be encountered during the development of hypertension as a response to oxidative stress. Statins may reduce the risk of developing hypertension and ocular diseases. We evaluate the effects of rosuvastatin (ROSU) on retinal functionality and oxidative stress levels in normotensive and spontaneously hypertensive rats (SHR). Wistar Kyoto (WKY) and SHR were treated for 3 weeks with rosuvastatin (10 mg kg(-1) day(-1)). Electroretinograms (ERG) were recorded before and after rosuvastatin treatment. Reactive oxygen species (ROS) were determined in the retina with dihydroethidium staining and NAD(P)H oxidase activity was evaluated. Retinal ganglion cell ROS and retinal NAD(P)H oxidase activity were higher in SHR than in WKY rats, respectively (17.1+/-1.1 vs 10.2+/-1.2 AU, P<0.01; 38095+/-8900 vs 14081+/-5820 RLU mg(-1); P<0.05). The ERG b-wave amplitude in SHR was significantly lower than that in WKY rats. Rosuvastatin reduced SBP in SHR but did not change plasma lipid levels. Rosuvastatin treatment in SHR significantly decreased ROS levels (11.2+/-1.3, P<0.01), NAD(P)H activity in retinal ganglion cells (9889+/-4290; P<0.05), and increased retinal plasmalogen content in SHR, but did not modify the ERG response. Rosuvastatin, beyond lowering cholesterol levels, was able to lower ROS in the retina induced by hypertension, but without improving retinal function in SHR. These findings point to a complex relationship between ROS in the pathogenesis of retinal disease and hypertension.