PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 23648561-4 2013 Rosuvastatin maintain the balance between oxidant generation and oxidant scavenging by reducing NADPH (nicotinamide adenine dinucleotide phosphate)-dependent production of reactive oxygen species, suppressing endothelial nitric oxide synthase (eNOS) uncoupling, inducing and upregulating antioxidant defense mechanism. Rosuvastatin Calcium 0-12 nitric oxide synthase 3 Homo sapiens 209-242 25453767-0 2015 HMG-CoA reductase inhibitor rosuvastatin improves abnormal brain electrical activity via mechanisms involving eNOS. Rosuvastatin Calcium 28-40 nitric oxide synthase 3 Homo sapiens 110-114 25453767-7 2015 However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs. Rosuvastatin Calcium 67-79 nitric oxide synthase 3 Homo sapiens 193-226 25453767-7 2015 However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs. Rosuvastatin Calcium 67-79 nitric oxide synthase 3 Homo sapiens 228-232 25453767-8 2015 Inhibition of eNOS activity with L-NG-Nitroarginine Methyl Ester (L-NAME) reversed the anti-epileptic effect of rosuvastatin significantly. Rosuvastatin Calcium 112-124 nitric oxide synthase 3 Homo sapiens 14-18 25453767-10 2015 Here, we provide evidence that among HMG-CoA reductase inhibitors, rosuvastatin was the most effective statin on the reduction of epileptiform activity, which was associated with improved BBB permeability, increased expression of eNOS and decreased expressions of pro-apoptotic p53, Bax and caspase-3. Rosuvastatin Calcium 67-79 nitric oxide synthase 3 Homo sapiens 230-234 25453767-11 2015 Our observation also revealed that the anti-epileptic effect of rosuvastatin was dependent on the increased expression level of eNOS. Rosuvastatin Calcium 64-76 nitric oxide synthase 3 Homo sapiens 128-132 27563480-0 2016 Impact of Rosuvastatin Treatment on HDL-Induced PKC-betaII and eNOS Phosphorylation in Endothelial Cells and Its Relation to Flow-Mediated Dilatation in Patients with Chronic Heart Failure. Rosuvastatin Calcium 10-22 nitric oxide synthase 3 Homo sapiens 63-67 27563480-5 2016 The aim of this study was to elucidate the impact of rosuvastatin on HDL mediated eNOS and PKC-betaII phosphorylation and its relation to endothelial function. Rosuvastatin Calcium 53-65 nitric oxide synthase 3 Homo sapiens 82-86 22799578-5 2012 RESULTS: Rosuvastatin treatment of human umbilical vein endothelial cells (ECs) enhanced the enzymatic activity of endothelial nitric oxide synthase (eNOS) and the expression of 78 S-nitrosoproteins. Rosuvastatin Calcium 9-21 nitric oxide synthase 3 Homo sapiens 115-148 23768697-12 2013 Western blot analysis further showed an earlier and greater S633 phosphorylation than that of S1177 in endothelial nitric oxide synthase after rosuvastatin treatment. Rosuvastatin Calcium 143-155 nitric oxide synthase 3 Homo sapiens 103-136 16165089-0 2005 Blockade of geranylgeranylation by rosuvastatin upregulates eNOS expression in human venous endothelial cells. Rosuvastatin Calcium 35-47 nitric oxide synthase 3 Homo sapiens 60-64 17928646-2 2007 Based on the differences between hydrophobic and hydrophilic statins in their reduction of cardiac events, we analyzed the effects of rosuvastatin and cerivastatin on eNOS and inducible NO synthase (iNOS) expression and NOS activity in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC). Rosuvastatin Calcium 134-146 nitric oxide synthase 3 Homo sapiens 167-171 17928646-7 2007 Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis. Rosuvastatin Calcium 0-12 nitric oxide synthase 3 Homo sapiens 102-106 18162361-3 2009 Rosuvastatin rapidly phosphorylated Akt and endothelial nitric oxide synthase (eNOS) in human endothelial cells. Rosuvastatin Calcium 0-12 nitric oxide synthase 3 Homo sapiens 44-77 17357484-10 2006 Consequently, the mechanisms of rosuvastatin"s neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3. Rosuvastatin Calcium 32-44 nitric oxide synthase 3 Homo sapiens 119-123 16165089-4 2005 In a concentration-dependent manner, rosuvastatin upregulated eNOS mRNA and protein expression. Rosuvastatin Calcium 37-49 nitric oxide synthase 3 Homo sapiens 62-66 16165089-5 2005 The effects on eNOS expression mediated through rosuvastatin could be reversed by treatment with mevalonate indicating inhibition of HMG-CoA reductase as the underlying mechanism. Rosuvastatin Calcium 48-60 nitric oxide synthase 3 Homo sapiens 15-19 16165089-6 2005 Treatment with geranylgeranylpyrophosphate, but not farnesylpyrophosphate, reversed the increase of eNOS expression induced by rosuvastatin. Rosuvastatin Calcium 127-139 nitric oxide synthase 3 Homo sapiens 100-104