Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the effect and mechanism of action of rosuvastatin on atherosclerotic lesion in a Wistar rat model, 16 Wistar rats were fed a cholesterol-rich, vitamin D3 overload diet and underwent balloon injury of the aorta. One day prior to injury, half of the rats began rosuvastatin treatment (5mg/kg/d) via oral gavage. Eight control rats received a basal diet and sham operation. After 14 weeks of treatment, the animals were sacrificed. Blood was collected to measure lipid and angiotensin II (Ang II) levels and morphologic analysis was performed on the aorta. Scavenger receptor-class B type I (SR-BI), Ang II type-1 (AT1) receptor and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK1/2) protein and mRNA levels were measured via Western blot and real time reverse transcriptase polymerase chain reaction, respectively. Spearman's rank correlation was utilized to examine the relationships between SR-BI and Ang II or AT1 receptor expression. The atherosclerosis model group demonstrated an increase in plasma lipid levels and aortic plaque formation. After 14 weeks of treatment with rosuvastatin, there was a significant decrease in plasma lipid and Ang II levels accompanied by an improvement in aortic lesions. Rosuvastatin increased the expression of SR-BI but significantly inhibited the expression of AT1 receptor and p-ERK1/2. SR-BI protein expression was inversely correlated with both the level of Ang II and expression of the AT1 receptor. In conclusion, rosuvastatin attenuates atherosclerosis in the Wistar rat model, and its anti-atherosclerotic activity may be through upregulation of SR-BI expression and inhibition of p-ERK1/2 levels and AT1 receptor expression.
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PMID:Rosuvastatin attenuates atherosclerosis in rats via activation of scavenger receptor class B type I. 2433 76

The efficacy and safety of different statins for human immunodeficiency virus (HIV)-positive patients in the primary prevention setting remain to be established. In the present meta-analysis, 18 studies with 736 HIV-positive patients receiving combination antiretroviral therapy (cART) and treated with statins in the primary prevention setting were included (21.0% women, median age 44.1 years old). The primary endpoint was the effect of statin therapy on total cholesterol (TC) levels. Rosuvastatin 10 mg and atorvastatin 10 mg provided the largest reduction in TC levels [mean -1.67, 95% confidence interval (CI) (-1.99, -1.35) mmol/L; and mean -1.44, 95% CI (-1.85, -1.02) mmol/L, respectively]. Atorvastatin 80 mg and simvastatin 20 mg provided the largest reduction in low-density lipoprotein (LDL) [mean -2.10, 95% CI (-3.39, -0.81) mmol/L; and mean -1.57, 95% CI (-2.67, -0.47) mmol/L, respectively]. Pravastatin 10-20 mg [mean 0.24, 95% CI (0.10, 0.38) mmol/L] and atorvastatin 10 mg [mean 0.15, 95% CI (0.007, 0.23) mmol/L] had the largest increase in high-density lipoprotein, whereas atorvastatin 80 mg [mean -0.60, 95% CI (-1.09, -0.11) mmol/L] and simvastatin 20 mg [mean -0.61, 95% CI (-1.14, -0.08) mmol/L] had the largest reduction in triglycerides. The mean discontinuation rate was 0.12 per 100 person-years [95% CI (0.05, 0.20)], and was higher with atorvastatin 10 mg [26.5 per 100 person-years, 95% CI (-13.4, 64.7)]. Meta-regression revealed that nucleoside reverse transcriptase inhibitors-sparing regimens were associated with reduced efficacy for statin's ability to lower TC. Statin therapy significantly lowers plasma TC and LDL levels in HIV-positive patients and is associated with low rates of adverse events. Statins are effective and safe when dose-adjusted for drug-drug interactions with cART.
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PMID:Comparative safety and efficacy of statins for primary prevention in human immunodeficiency virus-positive patients: a systematic review and meta-analysis. 2685 3

To begin developing a silk fibroin (SF) nanofibrous scaffolds that could promote osteogenesis, whilst enabling to deliver an active amount of Rosuvastatin (RSV) to the cells in long-time period, the present study aims to immobilize RSV onto the SF nanofibers through the argon radio frequency. Thus, the effect of plasma exposure times (0, 1, 3, and 5 min) was investigated on the morphology, loading efficiency, release profile, and osteogenesis activity. The successful loading of RSV on the SF nanofibers was proved by Fourier transformed infrared spectroscopy, Differential scanning calorimetry, and energy dispersive spectroscopy. In vitro drug release studies demonstrated that the RSV release was prolonged over a period of 21 d for plasma treated mats, while the non-plasma treated samples released the whole drug after 72 h. Moreover, the dose of RSV was controlled by the plasma exposure times, in which the highest amount of the released RSV was achieved after 3 min exposing to plasma. As suggested by MTT assay, the released amounts of RSV had no toxicity on the seeded human adipose tissue-derived stem cells and enhanced their proliferation. Moreover, using real-time reverse transcriptase-polymerase chain reaction and alizarin red staining proved that RSV-immobilized SF mats stimulate both early and late osteogenic gene differentiation in comparison with pure SF nanofibers. However, the highest differentiation was observed on the SF nanofibers treated with argon plasma for 3 min. The results support the potential of plasma treatment on sustained release of the RSV from SF nanofibers for osteogenesis enhancement.
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PMID:Osteogenic potential of Rosuvastatin immobilized on silk fibroin nanofibers using argon plasma treatment. 3052 38