PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 33930349-5 2021 We found that various statins, including pitavastatin, atorvastatin, fluvastatin, and lovastatin, but not squalene synthase inhibitor, repressed IL-1beta release upon MWCNT stimulation. Fluvastatin 69-80 interleukin 1 alpha Mus musculus 145-153 33893908-8 2021 The growth-inhibitory effects of fluvastatin were mediated through increased FAS/FASL mediated apoptotic cell death that was characterized by increased cleaved PARP and driven in part by depletion of an isoprenoid, geranyl geranyl pyrophosphate (GGPP). Fluvastatin 33-44 Fas ligand (TNF superfamily, member 6) Mus musculus 81-85 34032975-0 2021 Fluvastatin attenuated ischemia/reperfusion-induced autophagy and apoptosis in cardiomyocytes through down-regulation HMGB1/TLR4 signaling pathway. Fluvastatin 0-11 high mobility group box 1 Rattus norvegicus 118-123 34032975-0 2021 Fluvastatin attenuated ischemia/reperfusion-induced autophagy and apoptosis in cardiomyocytes through down-regulation HMGB1/TLR4 signaling pathway. Fluvastatin 0-11 toll-like receptor 4 Rattus norvegicus 124-128 34032975-2 2021 Previous reports demonstrated that fluvastatin pretreatment protected against myocardial ischemia/reperfusion (I/R) by inhibiting TLR4 signaling pathway and/or reducing proinflammatory cytokines. Fluvastatin 35-46 toll-like receptor 4 Rattus norvegicus 130-134 33602786-5 2021 Consistent with this cooperative model between the two spatially separated levels of protein N-glycosylation, fluvastatin-induced tumor cell death was enhanced by loss of Golgi-associated N-acetylglucosaminyltransferases MGAT1 or MGAT5. Fluvastatin 110-121 alpha-1,3-mannosyl-glycoprotein 2-beta-N-acetylglucosaminyltransferase Homo sapiens 221-226 33602786-5 2021 Consistent with this cooperative model between the two spatially separated levels of protein N-glycosylation, fluvastatin-induced tumor cell death was enhanced by loss of Golgi-associated N-acetylglucosaminyltransferases MGAT1 or MGAT5. Fluvastatin 110-121 alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase Homo sapiens 230-235 33880760-1 2021 The objective of this study was to determine the effects of the OATP inhibitor rifampin on pharmacokinetic of Biopharmaceutics Drug Disposition Classification System (BDDCS) Class 1 compound fluvastatin. Fluvastatin 191-202 solute carrier organic anion transporter family member 1A2 Homo sapiens 64-68 34032975-4 2021 This study aims to evaluate whether the cardioprotective role of fluvastatin in I/R is mediated by high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) pathway via anti-apoptotic and anti-autophagic functions. Fluvastatin 65-76 high mobility group box 1 Rattus norvegicus 99-124 34032975-4 2021 This study aims to evaluate whether the cardioprotective role of fluvastatin in I/R is mediated by high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) pathway via anti-apoptotic and anti-autophagic functions. Fluvastatin 65-76 high mobility group box 1 Rattus norvegicus 126-131 34032975-4 2021 This study aims to evaluate whether the cardioprotective role of fluvastatin in I/R is mediated by high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) pathway via anti-apoptotic and anti-autophagic functions. Fluvastatin 65-76 toll-like receptor 4 Rattus norvegicus 133-153 34032975-4 2021 This study aims to evaluate whether the cardioprotective role of fluvastatin in I/R is mediated by high-mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4) pathway via anti-apoptotic and anti-autophagic functions. Fluvastatin 65-76 toll-like receptor 4 Rattus norvegicus 155-159 34032975-8 2021 It was found that fluvastatin preconditioning improved left ventricular dysfunction, reduced HMGB1/TLR4/NF-kappaB expressions, and inhibited cardiomyocyte apoptosis, autophagy, and inflammation reaction. Fluvastatin 18-29 high mobility group box 1 Rattus norvegicus 93-98 34032975-8 2021 It was found that fluvastatin preconditioning improved left ventricular dysfunction, reduced HMGB1/TLR4/NF-kappaB expressions, and inhibited cardiomyocyte apoptosis, autophagy, and inflammation reaction. Fluvastatin 18-29 toll-like receptor 4 Rattus norvegicus 99-103 34032975-10 2021 Our findings indicate that fluvastatin exerts beneficial effects on cardiac ischemic damage, which may be associated with its anti-autophagic and anti-apoptotic functions via inhibition of HMGB1/TLR4-related pathway during I/R injury. Fluvastatin 27-38 high mobility group box 1 Rattus norvegicus 189-194 34032975-10 2021 Our findings indicate that fluvastatin exerts beneficial effects on cardiac ischemic damage, which may be associated with its anti-autophagic and anti-apoptotic functions via inhibition of HMGB1/TLR4-related pathway during I/R injury. Fluvastatin 27-38 toll-like receptor 4 Rattus norvegicus 195-199 33964033-13 2021 Fluvastatin reduced IL8, IL6, CCL21, AQP9 (p<0.001) and MMP9 (p<0.05) in the ex-vivo pulpitis model, while dequalinium chloride reduced AQP9 (p<0.001) but had no significant effect on the other biomarkers. Fluvastatin 0-11 C-X-C motif chemokine ligand 8 Homo sapiens 20-23 33964033-13 2021 Fluvastatin reduced IL8, IL6, CCL21, AQP9 (p<0.001) and MMP9 (p<0.05) in the ex-vivo pulpitis model, while dequalinium chloride reduced AQP9 (p<0.001) but had no significant effect on the other biomarkers. Fluvastatin 0-11 interleukin 6 Homo sapiens 25-28 33964033-13 2021 Fluvastatin reduced IL8, IL6, CCL21, AQP9 (p<0.001) and MMP9 (p<0.05) in the ex-vivo pulpitis model, while dequalinium chloride reduced AQP9 (p<0.001) but had no significant effect on the other biomarkers. Fluvastatin 0-11 C-C motif chemokine ligand 21 Homo sapiens 30-35 33964033-13 2021 Fluvastatin reduced IL8, IL6, CCL21, AQP9 (p<0.001) and MMP9 (p<0.05) in the ex-vivo pulpitis model, while dequalinium chloride reduced AQP9 (p<0.001) but had no significant effect on the other biomarkers. Fluvastatin 0-11 aquaporin 9 Homo sapiens 37-41 33964033-13 2021 Fluvastatin reduced IL8, IL6, CCL21, AQP9 (p<0.001) and MMP9 (p<0.05) in the ex-vivo pulpitis model, while dequalinium chloride reduced AQP9 (p<0.001) but had no significant effect on the other biomarkers. Fluvastatin 0-11 matrix metallopeptidase 9 Homo sapiens 56-60 34040513-9 2021 The most common medications coprescribed with DPP4is over all person-quarters were acetaminophen, simvastatin, fluvastatin, and colchicine (all >20,000 person-quarters). Fluvastatin 111-122 dipeptidyl peptidase 4 Homo sapiens 46-50 33893908-8 2021 The growth-inhibitory effects of fluvastatin were mediated through increased FAS/FASL mediated apoptotic cell death that was characterized by increased cleaved PARP and driven in part by depletion of an isoprenoid, geranyl geranyl pyrophosphate (GGPP). Fluvastatin 33-44 poly (ADP-ribose) polymerase family, member 1 Mus musculus 160-164 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 14-25 lectin, galactose binding, soluble 7 Mus musculus 43-53 33633571-0 2020 Cytotoxic and Pro-Apoptotic Effects of a Sub-Toxic Concentration of Fluvastatin on OVCAR3 Ovarian Cancer Cells After its Optimized Formulation to Melittin Nano-Conjugates. Fluvastatin 68-79 carbonic anhydrase 3 Homo sapiens 83-89 33633571-0 2020 Cytotoxic and Pro-Apoptotic Effects of a Sub-Toxic Concentration of Fluvastatin on OVCAR3 Ovarian Cancer Cells After its Optimized Formulation to Melittin Nano-Conjugates. Fluvastatin 68-79 melittin Apis mellifera 146-154 33633571-1 2020 Fluvastatin (FLV) is a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor often used to lower total and low-density lipoprotein (LDL) cholesterol and for the prevention of adverse cardiovascular events. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 23-75 33633571-1 2020 Fluvastatin (FLV) is a hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor often used to lower total and low-density lipoprotein (LDL) cholesterol and for the prevention of adverse cardiovascular events. Fluvastatin 13-16 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 23-75 33633571-7 2020 The synergistic antineoplastic activity of FLV and MEL combined in the optimized formula was also showed by the marked pronecrotic and pro-apoptotic activities, the latter mediated by the modulation of BAX/BCL-2 ratio in favor of BAX. Fluvastatin 43-46 BCL2 associated X, apoptosis regulator Homo sapiens 202-205 33633571-7 2020 The synergistic antineoplastic activity of FLV and MEL combined in the optimized formula was also showed by the marked pronecrotic and pro-apoptotic activities, the latter mediated by the modulation of BAX/BCL-2 ratio in favor of BAX. Fluvastatin 43-46 BCL2 apoptosis regulator Homo sapiens 206-211 33633571-7 2020 The synergistic antineoplastic activity of FLV and MEL combined in the optimized formula was also showed by the marked pronecrotic and pro-apoptotic activities, the latter mediated by the modulation of BAX/BCL-2 ratio in favor of BAX. Fluvastatin 43-46 BCL2 associated X, apoptosis regulator Homo sapiens 230-233 33341662-7 2021 These results indicated that lactone forms of statins other than fluvastatin showed more potent inhibition of CYP2C9-catalyzed S-warfarin 7-hydroxylation than the corresponding acid forms. Fluvastatin 65-76 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 110-116 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 14-25 interleukin 6 Homo sapiens 187-191 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 14-25 C-X-C motif chemokine ligand 8 Homo sapiens 196-200 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 14-25 interleukin 17A Mus musculus 223-229 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 164-175 interleukin 6 Homo sapiens 187-191 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 164-175 C-X-C motif chemokine ligand 8 Homo sapiens 196-200 33055419-7 2021 We identified fluvastatin as an inducer of galectin-7 expression by connectivity map (cMAP) analysis, confirmed this effect in keratinocytes, and demonstrated that fluvastatin attenuated IL-6 and IL-8 production induced by IL-17A. Fluvastatin 164-175 interleukin 17A Mus musculus 223-229 33415155-0 2020 Fluvastatin-Pretreated Donor Cells Attenuated Murine aGVHD by Balancing Effector T Cell Distribution and Function under the Regulation of KLF2. Fluvastatin 0-11 Kruppel-like factor 2 (lung) Mus musculus 138-142 33415155-7 2020 Furthermore, evidence confirmed that Fluvastatin had a long-lasting effect to sustain KLF2 expression both in vitro and in vivo even under the stimulated circumstance. Fluvastatin 37-48 Kruppel-like factor 2 (lung) Mus musculus 86-90 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 selectin, lymphocyte Mus musculus 108-113 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 chemokine (C-C motif) receptor 7 Mus musculus 118-122 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 chemokine (C-X-C motif) receptor 3 Mus musculus 150-155 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 CD44 antigen Mus musculus 160-164 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 Kruppel-like factor 2 (lung) Mus musculus 200-221 33415155-5 2020 The potential mechanism of correcting the effector T cell biased distribution was that Fluvastatin elevated CD62L and CCR7 expression while decreased CXCR3 and CD44 levels, which were correlated with Kruppel-like factor 2 (KLF2) sustention in donor-derived cells. Fluvastatin 87-98 Kruppel-like factor 2 (lung) Mus musculus 223-227 33415155-6 2020 In addition, Fluvastatin was contributed to reducing cytokines IFN-gamma, TNF-alpha, and granzyme-B production in allogeneic effector CD4+ and CD8+ T cells. Fluvastatin 13-24 interferon gamma Mus musculus 63-72 33415155-6 2020 In addition, Fluvastatin was contributed to reducing cytokines IFN-gamma, TNF-alpha, and granzyme-B production in allogeneic effector CD4+ and CD8+ T cells. Fluvastatin 13-24 tumor necrosis factor Mus musculus 74-83 33415155-6 2020 In addition, Fluvastatin was contributed to reducing cytokines IFN-gamma, TNF-alpha, and granzyme-B production in allogeneic effector CD4+ and CD8+ T cells. Fluvastatin 13-24 granzyme B Mus musculus 89-99 32203069-11 2020 The mean fluvastatin concentration measured in the serum was 0.2 muM (range: 0.0-1.1 muM), and in prostatic tissue was 8.5 nM (range: 0.0-77.0 nM). Fluvastatin 9-20 latexin Homo sapiens 65-68 32203069-11 2020 The mean fluvastatin concentration measured in the serum was 0.2 muM (range: 0.0-1.1 muM), and in prostatic tissue was 8.5 nM (range: 0.0-77.0 nM). Fluvastatin 9-20 latexin Homo sapiens 85-88 33250768-5 2020 Furthermore, we found that the expression of PTTG1 was markedly suppressed by lipophilic statins, such as simvastatin, fluvastatin, mevastatin, and lovastatin, but not by hydrophilic pravastatin. Fluvastatin 119-130 PTTG1 regulator of sister chromatid separation, securin Homo sapiens 45-50 33255298-1 2020 Fluvastatin (FLUVA), which is a common anti-hypercholesterolemia drug, exhibits potential anticancer activity as it suppresses the proliferation, angiogenesis, and metastasis of breast cancer cells via inhibiting 3-hydroxy-methyl glutaryl-coenzyme A (HMG-CoA) reductase. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 230-269 33255298-1 2020 Fluvastatin (FLUVA), which is a common anti-hypercholesterolemia drug, exhibits potential anticancer activity as it suppresses the proliferation, angiogenesis, and metastasis of breast cancer cells via inhibiting 3-hydroxy-methyl glutaryl-coenzyme A (HMG-CoA) reductase. Fluvastatin 13-18 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 230-269 33224343-6 2020 According to the above-mentioned results, rosuvastatin, fluvastatin, pitavastatin and atorvastatin were found to have stronger binding to CRP compared with the standard ligand phosphocholine (pKi = 14.55). Fluvastatin 56-67 C-reactive protein Homo sapiens 138-141 32348623-12 2020 Findings indicate TSP-5 and fluvastatin have a protective effect on ECs, being proangiogenic and reversing the antiangiogenic effects of TSP-1 and TSP-2. Fluvastatin 28-39 thrombospondin 1 Homo sapiens 137-142 32718595-4 2020 The maximum swelling ratio (1000.0 %) was optimized at pH 10, 180 min and 25 C. The validity of NFe3O4@Zn(GA)/Starch-Hydrogel for adsorptive removal of Fluvastatin statin drug provided maximum equilibrium adsorption capacity 782.05 mg g-1. Fluvastatin 153-164 nuclear receptor subfamily 2 group F member 2 Homo sapiens 97-101 32348623-12 2020 Findings indicate TSP-5 and fluvastatin have a protective effect on ECs, being proangiogenic and reversing the antiangiogenic effects of TSP-1 and TSP-2. Fluvastatin 28-39 thrombospondin 2 Homo sapiens 147-152 32237049-9 2020 These data indicated that FLU and EVR suppressed IFN-gamma-induced HLA-DR expression at the transcriptional and post-translational level, respectively, suggesting a potential approach for alleviating DSA-related issues in organ transplantation. Fluvastatin 26-29 interferon gamma Homo sapiens 49-58 32729746-4 2020 Fluvastatin is metabolized by CYP2C9, whereas pravastatin, rosuvastatin, and pitavastatin are unaffected by inhibition by either CYP. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 30-36 32422132-0 2020 Fluvastatin prevents the development of arthritis in env-pX rats via up- regulation of Rho GTPase-activating protein 12. Fluvastatin 0-11 Rho GTPase activating protein 12 Rattus norvegicus 87-119 32422132-9 2020 Comprehensive serum exosomal miRNA analysis suggested that the expression of Rho GTPase-activating protein 12 (Arhgap12) was decreased in arthritic env-pX rats but increased with the administration of fluvastatin. Fluvastatin 201-212 Rho GTPase activating protein 12 Rattus norvegicus 77-109 32422132-9 2020 Comprehensive serum exosomal miRNA analysis suggested that the expression of Rho GTPase-activating protein 12 (Arhgap12) was decreased in arthritic env-pX rats but increased with the administration of fluvastatin. Fluvastatin 201-212 Rho GTPase activating protein 12 Rattus norvegicus 111-119 32422132-11 2020 The collective findings suggest that fluvastatin prevents the development of arthritis in env-pX rats via the up-regulation of ARHGAP12. Fluvastatin 37-48 Rho GTPase activating protein 12 Rattus norvegicus 127-135 32434944-8 2020 Complementing these data, we found that p53 deficiency or Bcl-2 overexpression reduced fluvastatin-induced apoptosis. Fluvastatin 87-98 tumor protein p53 Homo sapiens 40-43 32434944-8 2020 Complementing these data, we found that p53 deficiency or Bcl-2 overexpression reduced fluvastatin-induced apoptosis. Fluvastatin 87-98 BCL2 apoptosis regulator Homo sapiens 58-63 32434944-11 2020 SIGNIFICANCE STATEMENT: Fluvastatin, a statin drug used to lower cholesterol, induces apoptosis in primary and transformed mast cells by antagonizing protein isoprenylation, effectively inhibiting stem cell factor (SCF)-induced survival signals. Fluvastatin 24-35 KIT ligand Homo sapiens 197-213 32434944-11 2020 SIGNIFICANCE STATEMENT: Fluvastatin, a statin drug used to lower cholesterol, induces apoptosis in primary and transformed mast cells by antagonizing protein isoprenylation, effectively inhibiting stem cell factor (SCF)-induced survival signals. Fluvastatin 24-35 KIT ligand Homo sapiens 215-218 33214841-0 2020 Structural Basis for Activation of Human Sirtuin 6 by Fluvastatin. Fluvastatin 54-65 sirtuin 6 Homo sapiens 41-50 33214841-4 2020 Sirt6 deacetylase activity can be stimulated with small molecules, and fluvastatin, an FDA-approved synthetic statin, was recently described as a novel Sirt6 activator. Fluvastatin 71-82 sirtuin 6 Homo sapiens 152-157 33214841-5 2020 We studied the molecular details of this effect on Sirt6 in deacylation assays and by solving a crystal structure of a Sirt6/fluvastatin complex. Fluvastatin 125-136 sirtuin 6 Homo sapiens 119-124 33214841-6 2020 We find that fluvastatin inhibits Sirt1-3 at higher concentrations but has a unique, activating effect on Sirt6. Fluvastatin 13-24 sirtuin 1 Homo sapiens 34-41 33214841-6 2020 We find that fluvastatin inhibits Sirt1-3 at higher concentrations but has a unique, activating effect on Sirt6. Fluvastatin 13-24 sirtuin 6 Homo sapiens 106-111 33214841-7 2020 The complex structure reveals that fluvastatin occupies the Sirt6 substrate acyl channel exit, similar to other, unrelated activator families, providing interaction details that will support the development of potent, druglike Sirt6 activators. Fluvastatin 35-46 sirtuin 6 Homo sapiens 60-65 33214841-7 2020 The complex structure reveals that fluvastatin occupies the Sirt6 substrate acyl channel exit, similar to other, unrelated activator families, providing interaction details that will support the development of potent, druglike Sirt6 activators. Fluvastatin 35-46 sirtuin 6 Homo sapiens 227-232 32373204-8 2020 It suggests that the increased effect of SLCO1B1 T521C genotype on ER formulation of fluvastatin was mainly caused by lower blood concentrations. Fluvastatin 85-96 solute carrier organic anion transporter family member 1B1 Homo sapiens 41-48 32083311-14 2020 Fluvastatin-mediated cholesterol depletion (-27.8%) lowered VSMC migration distance on fibronectin (FN) coated surface (-14.8%) but not on type 1 collagen (COL1) coated surface. Fluvastatin 0-11 fibronectin 1 Rattus norvegicus 87-98 32083311-14 2020 Fluvastatin-mediated cholesterol depletion (-27.8%) lowered VSMC migration distance on fibronectin (FN) coated surface (-14.8%) but not on type 1 collagen (COL1) coated surface. Fluvastatin 0-11 fibronectin 1 Rattus norvegicus 100-102 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 fms related receptor tyrosine kinase 3 Homo sapiens 23-27 32104271-0 2020 Fluvastatin protects myocardial cells in mice with acute myocardial infarction through inhibiting RhoA/ROCK pathway. Fluvastatin 0-11 ras homolog family member A Mus musculus 98-102 32104271-0 2020 Fluvastatin protects myocardial cells in mice with acute myocardial infarction through inhibiting RhoA/ROCK pathway. Fluvastatin 0-11 Rho-associated coiled-coil containing protein kinase 1 Mus musculus 103-107 32104271-9 2020 After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Fluvastatin 94-97 ras homolog family member A Mus musculus 10-22 32104271-9 2020 After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Fluvastatin 94-97 ras homolog family member A Mus musculus 24-28 32104271-9 2020 After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Fluvastatin 94-97 Rho-associated coiled-coil containing protein kinase 1 Mus musculus 30-34 32104271-9 2020 After the Rho member A (RhoA)/ROCK pathway agonist Ang II was added, the mitigation effect of Flu on myocardial apoptosis in the infarction region in AMI mice was evidently weakened. Fluvastatin 94-97 angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus 51-57 32104271-10 2020 Flu mitigates AMI-induced myocardial apoptosis in mice, and the possible mechanism is that the inflammatory and oxidative stress responses activated and mediated by RhoA/ROCK are effectively inhibited. Fluvastatin 0-3 ras homolog family member A Mus musculus 165-169 32104271-10 2020 Flu mitigates AMI-induced myocardial apoptosis in mice, and the possible mechanism is that the inflammatory and oxidative stress responses activated and mediated by RhoA/ROCK are effectively inhibited. Fluvastatin 0-3 Rho-associated coiled-coil containing protein kinase 1 Mus musculus 170-174 31554629-4 2019 In this study, we found that fluvastatin targeted 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR), which a rate-limiting enzyme in the mevalonate pathway, and inhibited non-small cell lung cancer (NSCLC) tumorigenesis. Fluvastatin 29-40 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 109-114 31554629-6 2019 Knockdown of HMGCR in NSCLC cells attenuated growth and induced apoptosis in vitro and in vivo Furthermore, we found that fluvastatin, an inhibitor of HMGCR, suppressed NSCLC cell growth and induced apoptosis. Fluvastatin 122-133 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 13-18 31554629-6 2019 Knockdown of HMGCR in NSCLC cells attenuated growth and induced apoptosis in vitro and in vivo Furthermore, we found that fluvastatin, an inhibitor of HMGCR, suppressed NSCLC cell growth and induced apoptosis. Fluvastatin 122-133 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 151-156 31272229-0 2019 Fluvastatin attenuates doxorubicin-induced testicular toxicity in rats by reducing oxidative stress and regulating the blood-testis barrier via mTOR signaling pathway. Fluvastatin 0-11 mechanistic target of rapamycin kinase Rattus norvegicus 144-148 31272229-5 2019 In addition to its cholesterol-lowering effect, fluvastatin showed an antioxidant effect by cleaning hydroxyl and superoxide radicals and this drug could have a protective effect by acting on the mammalian target of rapamycin (mTOR) signal pathway in testicular damage caused by obesity. Fluvastatin 48-59 mechanistic target of rapamycin kinase Homo sapiens 196-225 31272229-5 2019 In addition to its cholesterol-lowering effect, fluvastatin showed an antioxidant effect by cleaning hydroxyl and superoxide radicals and this drug could have a protective effect by acting on the mammalian target of rapamycin (mTOR) signal pathway in testicular damage caused by obesity. Fluvastatin 48-59 mechanistic target of rapamycin kinase Homo sapiens 227-231 31272229-7 2019 The present study indicates that fluvastatin may have a protective and therapeutic effect by removing reactive oxygen species and by regulating the mTOR, connexin 43, and matrix metalloproteinase 9 protein and messenger ribonucleic acid expressions, which play an important role in regulating the blood-testis barrier. Fluvastatin 33-44 mechanistic target of rapamycin kinase Homo sapiens 148-152 31272229-7 2019 The present study indicates that fluvastatin may have a protective and therapeutic effect by removing reactive oxygen species and by regulating the mTOR, connexin 43, and matrix metalloproteinase 9 protein and messenger ribonucleic acid expressions, which play an important role in regulating the blood-testis barrier. Fluvastatin 33-44 gap junction protein alpha 1 Homo sapiens 154-165 31272229-7 2019 The present study indicates that fluvastatin may have a protective and therapeutic effect by removing reactive oxygen species and by regulating the mTOR, connexin 43, and matrix metalloproteinase 9 protein and messenger ribonucleic acid expressions, which play an important role in regulating the blood-testis barrier. Fluvastatin 33-44 matrix metallopeptidase 9 Homo sapiens 171-197 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 226-231 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 Pim-1 proto-oncogene, serine/threonine kinase Homo sapiens 281-286 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 heat shock protein 90 alpha family class A member 1 Homo sapiens 311-316 31533545-5 2019 Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3. Fluvastatin 165-176 fms related receptor tyrosine kinase 3 Homo sapiens 124-128 31023626-11 2019 Overcoming this feedback mechanism by knocking down or inhibiting SREBP2 potentiated fluvastatin-induced PCa cell death. Fluvastatin 85-96 sterol regulatory element binding transcription factor 2 Homo sapiens 66-72 32245297-7 2019 The results indicated that IFN-lambda +fluvastatin acted as an inhibitor in mRNA expression of SREBP1c; while acting as an inducer in the expression of ABCA-1. Fluvastatin 39-50 interferon alpha 1 Homo sapiens 27-30 32245297-7 2019 The results indicated that IFN-lambda +fluvastatin acted as an inhibitor in mRNA expression of SREBP1c; while acting as an inducer in the expression of ABCA-1. Fluvastatin 39-50 sterol regulatory element binding transcription factor 1 Homo sapiens 95-102 32245297-7 2019 The results indicated that IFN-lambda +fluvastatin acted as an inhibitor in mRNA expression of SREBP1c; while acting as an inducer in the expression of ABCA-1. Fluvastatin 39-50 ATP binding cassette subfamily A member 1 Homo sapiens 152-158 32245297-8 2019 The results of ABCA1 assay showed a significant increase of this protein after treatment with fluvastatin and IFN-lambda compared with untreated cells (p=0.02). Fluvastatin 94-105 ATP binding cassette subfamily A member 1 Homo sapiens 15-20 32245297-9 2019 Moreover, the mRNA expression of HCV core was suppressed in all experimental groups treated with fluvastatin, IFN-lambda or their combination which was more significant after treatment with fluvastatin+IFN-lambda (p<0.001). Fluvastatin 190-201 interferon alpha 1 Homo sapiens 110-113 31023626-5 2019 The response of PCa cell lines to fluvastatin-mediated HMGCR inhibition was assessed using cell viability and apoptosis assays. Fluvastatin 34-45 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 55-60 30989645-5 2019 A candidate gene analysis suggested that CYP2C9*2 also affects the AUC of both fluvastatin enantiomers and that SLCO2B1 single-nucleotide variations may affect the AUC of 3S,5R-fluvastatin. Fluvastatin 79-90 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 41-47 30989645-7 2019 Genotyping of both CYP2C9 and SLCO1B1 may be useful in predicting fluvastatin efficacy and myotoxicity. Fluvastatin 66-77 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 19-25 30989645-7 2019 Genotyping of both CYP2C9 and SLCO1B1 may be useful in predicting fluvastatin efficacy and myotoxicity. Fluvastatin 66-77 solute carrier organic anion transporter family member 1B1 Homo sapiens 30-37 30920401-7 2019 Intriguingly, application of a statin-related drug, fluvastatin, also resulted in a synergistic increase of sensitivity to vemurafenib in the VR cells (combination index: 0.73-0.86) probably by alleviating constitutive AKT activation, whereas the same treatment did not notably alter the vemurafenib sensitivity of the parental cells. Fluvastatin 52-63 AKT serine/threonine kinase 1 Homo sapiens 219-222 30882968-7 2019 We then showed that CD10 and CD11 are efficient chiral selectors for the capillary electrophoretic separation of the enantiomeric pharmaceuticals fluvastatin, mefloquine, carvedilol, and primaquine. Fluvastatin 146-157 membrane metalloendopeptidase Homo sapiens 20-24 31013989-11 2019 We showed that low-dose fluvastatin and valsartan, separately and in combination, substantially increase expression of SIRT1, PRKAA, and KLOTHO genes, which may be attributed to their so far unreported pleiotropic beneficial effects. Fluvastatin 24-35 sirtuin 1 Homo sapiens 119-124 30939155-0 2019 Regulatory mechanisms of fluvastatin and lovastatin for the p21 induction in human cervical cancer HeLa cells. Fluvastatin 25-36 H3 histone pseudogene 16 Homo sapiens 60-63 31013989-11 2019 We showed that low-dose fluvastatin and valsartan, separately and in combination, substantially increase expression of SIRT1, PRKAA, and KLOTHO genes, which may be attributed to their so far unreported pleiotropic beneficial effects. Fluvastatin 24-35 protein kinase AMP-activated catalytic subunit alpha 2 Homo sapiens 126-131 31013989-11 2019 We showed that low-dose fluvastatin and valsartan, separately and in combination, substantially increase expression of SIRT1, PRKAA, and KLOTHO genes, which may be attributed to their so far unreported pleiotropic beneficial effects. Fluvastatin 24-35 klotho Homo sapiens 137-143 30939155-5 2019 Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. Fluvastatin 33-44 tumor protein p53 Homo sapiens 130-133 30939155-5 2019 Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells. Fluvastatin 33-44 H3 histone pseudogene 16 Homo sapiens 302-305 30939155-6 2019 The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner. Fluvastatin 93-104 H3 histone pseudogene 16 Homo sapiens 158-161 30557545-0 2019 Fluvastatin-mediated down-regulation of SATB1 affects aggressive phenotypes of human non-small-cell lung cancer cell line H292. Fluvastatin 0-11 SATB homeobox 1 Homo sapiens 40-45 30939798-5 2019 We paid particular attention to fluvastatin sodium (FS), because as an inhibitor of the cellular hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase, FS has already been approved for treatment of hypercholesteremia. Fluvastatin 32-50 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 97-150 30939798-5 2019 We paid particular attention to fluvastatin sodium (FS), because as an inhibitor of the cellular hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase, FS has already been approved for treatment of hypercholesteremia. Fluvastatin 52-54 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 97-150 30939798-6 2019 We found that in the cellular levels, FS treatment significantly increased UCP1 expression and BAT activity in human brown adipocytes. Fluvastatin 38-40 uncoupling protein 1 Homo sapiens 75-79 30898664-0 2019 Fluvastatin inhibits Rab5-mediated IKs internalization caused by chronic Ca2+-dependent PKC activation. Fluvastatin 0-11 RAB5A, member RAS oncogene family Homo sapiens 21-25 30898664-7 2019 Our data indicates fluvastatin inhibition of Rab5 restores channel localization and function after cPKC-mediated channel internalization. Fluvastatin 19-30 RAB5A, member RAS oncogene family Homo sapiens 45-49 30557545-7 2019 RT-PCR and Western blot were performed to examine the effects of fluvastatin on expression of SATB1 and Wnt/beta-catenin signaling components. Fluvastatin 65-76 SATB homeobox 1 Homo sapiens 94-99 30557545-7 2019 RT-PCR and Western blot were performed to examine the effects of fluvastatin on expression of SATB1 and Wnt/beta-catenin signaling components. Fluvastatin 65-76 catenin beta 1 Homo sapiens 108-120 30557545-9 2019 The expression of SATB1 was down-regulated by fluvastatin in a dose-dependent manner. Fluvastatin 46-57 SATB homeobox 1 Homo sapiens 18-23 30557545-13 2019 SIGNIFICANCE: We presented a possible mechanism of statins that fluvastatin significantly suppressed the in vitro tumor progression of H292 cells possibly by down-regulation of SATB1 via Wnt/beta-catenin pathway, which provided new therapeutic possibilities for more cancers driven by hyperexpression of SATB1 and Wnt/beta-catenin pathway. Fluvastatin 64-75 SATB homeobox 1 Homo sapiens 177-182 30557545-13 2019 SIGNIFICANCE: We presented a possible mechanism of statins that fluvastatin significantly suppressed the in vitro tumor progression of H292 cells possibly by down-regulation of SATB1 via Wnt/beta-catenin pathway, which provided new therapeutic possibilities for more cancers driven by hyperexpression of SATB1 and Wnt/beta-catenin pathway. Fluvastatin 64-75 catenin beta 1 Homo sapiens 191-203 30557545-13 2019 SIGNIFICANCE: We presented a possible mechanism of statins that fluvastatin significantly suppressed the in vitro tumor progression of H292 cells possibly by down-regulation of SATB1 via Wnt/beta-catenin pathway, which provided new therapeutic possibilities for more cancers driven by hyperexpression of SATB1 and Wnt/beta-catenin pathway. Fluvastatin 64-75 SATB homeobox 1 Homo sapiens 304-309 30557545-13 2019 SIGNIFICANCE: We presented a possible mechanism of statins that fluvastatin significantly suppressed the in vitro tumor progression of H292 cells possibly by down-regulation of SATB1 via Wnt/beta-catenin pathway, which provided new therapeutic possibilities for more cancers driven by hyperexpression of SATB1 and Wnt/beta-catenin pathway. Fluvastatin 64-75 catenin beta 1 Homo sapiens 318-330 30339864-8 2019 Net ERs of prazosin and fluvastatin, dual substrates of P-gp and BCRP, determined by dividing ERs in LLC-PK1-P-gp cells by those in LLC-PK1 WT cells, were <2, but increased to >2 in the presence of Ko143. Fluvastatin 24-35 phosphoglycolate phosphatase Sus scrofa 56-60 30851734-6 2019 Several statins, including atorvastatin, simvastatin, lovastatin, and fluvastatin, increased CD55 protein expression in astrocytes, including primary cultures, by three- to four-fold at 24 h, conferring significant protection against AQP4-IgG-induced CDC. Fluvastatin 70-81 CD55 molecule (Cromer blood group) Homo sapiens 93-97 30851734-6 2019 Several statins, including atorvastatin, simvastatin, lovastatin, and fluvastatin, increased CD55 protein expression in astrocytes, including primary cultures, by three- to four-fold at 24 h, conferring significant protection against AQP4-IgG-induced CDC. Fluvastatin 70-81 aquaporin 4 Homo sapiens 234-238 30339864-8 2019 Net ERs of prazosin and fluvastatin, dual substrates of P-gp and BCRP, determined by dividing ERs in LLC-PK1-P-gp cells by those in LLC-PK1 WT cells, were <2, but increased to >2 in the presence of Ko143. Fluvastatin 24-35 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 65-69 30339864-8 2019 Net ERs of prazosin and fluvastatin, dual substrates of P-gp and BCRP, determined by dividing ERs in LLC-PK1-P-gp cells by those in LLC-PK1 WT cells, were <2, but increased to >2 in the presence of Ko143. Fluvastatin 24-35 phosphoglycolate phosphatase Sus scrofa 109-113 30528195-3 2019 Mean area under the plasma concentration of atorvastatin, pitavastatin, and rosuvastatin in OATP1B1 *15/*15 were 2.2, 1.7 and 1.58-times greater than the corresponding values in OATP1B1 *1b/*1b, respectively, whereas that of fluvastatin was identical to those in other OATP1B1 genotypes. Fluvastatin 225-236 solute carrier organic anion transporter family member 1B1 Homo sapiens 92-99 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Fluvastatin 62-73 solute carrier organic anion transporter family member 1B1 Homo sapiens 151-158 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Fluvastatin 62-73 solute carrier organic anion transporter family member 1B3 Homo sapiens 160-167 30652318-5 2019 In contrast, atorvastatin, bosentan, etoposide, fexofenadine, fluvastatin, glibenclamide and simeprevir were broadly transported by recombinant monkey OATP1B1, OATP1B3 and OATP2B1. Fluvastatin 62-73 solute carrier organic anion transporter family member 2B1 Homo sapiens 172-179 30674312-6 2019 Network meta-analysis showed that Fluvastatin (97.7%), Atorvastatin (68.0%) and Rosuvastatin (49.3%) had higher cumulative probability than other statins in reducing CRP in COPD patients. Fluvastatin 34-45 C-reactive protein Homo sapiens 166-169 30674312-9 2019 In addition, Fluvastatin and Atorvastatin are more effective in reducing CRP and PH in COPD patients. Fluvastatin 13-24 C-reactive protein Homo sapiens 73-76 29482467-11 2018 CONCLUSION: Oral fluvastatin application could reduce formation of intra-abdominal adhesion by promoting expression of MMP-9 level, lowering the levels of IL-1beta and increasing the activity of t-PA after abdominal surgery. Fluvastatin 17-28 matrix metallopeptidase 9 Rattus norvegicus 119-124 30537987-9 2018 Indeed, we found fluvastatin-induced HMGCR transcript levels to be directly correlated with the degree of histological progression of lesions, indicating that the extent of cholesterol pathway suppression directly correlates with abrogation of the tumorigenic process. Fluvastatin 17-28 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 37-42 29482467-11 2018 CONCLUSION: Oral fluvastatin application could reduce formation of intra-abdominal adhesion by promoting expression of MMP-9 level, lowering the levels of IL-1beta and increasing the activity of t-PA after abdominal surgery. Fluvastatin 17-28 interleukin 1 beta Rattus norvegicus 155-163 29482467-11 2018 CONCLUSION: Oral fluvastatin application could reduce formation of intra-abdominal adhesion by promoting expression of MMP-9 level, lowering the levels of IL-1beta and increasing the activity of t-PA after abdominal surgery. Fluvastatin 17-28 plasminogen activator, tissue type Rattus norvegicus 195-199 30363031-1 2018 OBJECTIVE: The aim of this study was to determine the impact of the SLCO1B1, apolipoprotein E (ApoE), and CYP2C9 genotypes on the lipid-lowering efficacy of fluvastatin. Fluvastatin 157-168 apolipoprotein E Homo sapiens 77-93 30555540-0 2018 Erratum: Fluvastatin inhibits cardiomyocyte apoptosis after myocardial infarction through Toll pathway. Fluvastatin 9-20 toll like receptor 4 Homo sapiens 90-94 30363031-1 2018 OBJECTIVE: The aim of this study was to determine the impact of the SLCO1B1, apolipoprotein E (ApoE), and CYP2C9 genotypes on the lipid-lowering efficacy of fluvastatin. Fluvastatin 157-168 apolipoprotein E Homo sapiens 95-99 30363031-0 2018 The association between the SLCO1B1, apolipoprotein E, and CYP2C9 genes and lipid response to fluvastatin: a meta-analysis. Fluvastatin 94-105 solute carrier organic anion transporter family member 1B1 Homo sapiens 28-35 30363031-1 2018 OBJECTIVE: The aim of this study was to determine the impact of the SLCO1B1, apolipoprotein E (ApoE), and CYP2C9 genotypes on the lipid-lowering efficacy of fluvastatin. Fluvastatin 157-168 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 106-112 30363031-0 2018 The association between the SLCO1B1, apolipoprotein E, and CYP2C9 genes and lipid response to fluvastatin: a meta-analysis. Fluvastatin 94-105 apolipoprotein E Homo sapiens 37-53 30363031-0 2018 The association between the SLCO1B1, apolipoprotein E, and CYP2C9 genes and lipid response to fluvastatin: a meta-analysis. Fluvastatin 94-105 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 59-65 30363031-9 2018 CONCLUSION: The findings of this study suggested that the SLCO1B1 and ApoE polymorphisms could influence the lipid-lowering effect of fluvastatin, whereas the CYP2C9 genotypes were not associated with the therapeutic effects of fluvastatin. Fluvastatin 134-145 solute carrier organic anion transporter family member 1B1 Homo sapiens 58-65 30363031-1 2018 OBJECTIVE: The aim of this study was to determine the impact of the SLCO1B1, apolipoprotein E (ApoE), and CYP2C9 genotypes on the lipid-lowering efficacy of fluvastatin. Fluvastatin 157-168 solute carrier organic anion transporter family member 1B1 Homo sapiens 68-75 30363031-9 2018 CONCLUSION: The findings of this study suggested that the SLCO1B1 and ApoE polymorphisms could influence the lipid-lowering effect of fluvastatin, whereas the CYP2C9 genotypes were not associated with the therapeutic effects of fluvastatin. Fluvastatin 134-145 apolipoprotein E Homo sapiens 70-74 30142209-10 2018 In SAMP6, BMP2, Runx2 and Bglap2 mRNA and protein expressions were significantly increased by fluvastatin, and ALP activity was increased by BMP2 action. Fluvastatin 94-105 bone morphogenetic protein 2 Mus musculus 10-14 30216659-3 2018 The lipophilic fluvastatin, simvastatin, atorvastatin, and lovastatin as well as the nitrogenous BPs alendronate and ibandronate, but not hydrophilic pravastatin increased IL-33 mRNA and intracellular IL-33 protein levels in both human adult cardiac myocytes (HACM) and fibroblasts (HACF). Fluvastatin 15-26 interleukin 33 Homo sapiens 172-177 30216659-4 2018 Additionally, fluvastatin reduced soluble ST2 secretion from HACM. Fluvastatin 14-25 ST2 Homo sapiens 42-45 30078674-0 2018 Fluvastatin activates sirtuin 6 to regulate sterol regulatory element-binding proteins and AMP-activated protein kinase in HepG2 cells. Fluvastatin 0-11 sirtuin 6 Homo sapiens 22-31 30078674-6 2018 When HepG2 cells were treated with fluvastatin, the expression of SIRT6 and phosphorylation of sterol regulatory element-binding protein (SREBP)-1 and AMPKalpha, which is regulated by SIRT6, increased. Fluvastatin 35-46 sirtuin 6 Homo sapiens 66-71 30078674-6 2018 When HepG2 cells were treated with fluvastatin, the expression of SIRT6 and phosphorylation of sterol regulatory element-binding protein (SREBP)-1 and AMPKalpha, which is regulated by SIRT6, increased. Fluvastatin 35-46 sterol regulatory element binding transcription factor 1 Homo sapiens 95-146 30078674-6 2018 When HepG2 cells were treated with fluvastatin, the expression of SIRT6 and phosphorylation of sterol regulatory element-binding protein (SREBP)-1 and AMPKalpha, which is regulated by SIRT6, increased. Fluvastatin 35-46 sirtuin 6 Homo sapiens 184-189 30078674-7 2018 In this study, we examined the mechanism underlying cholesterol regulation by fluvastatin via SREBP-1 and AMPKalpha pathway and suggested that fluvastatin is an SIRT6 activator that regulates cholesterol homeostasis and fatty liver disease. Fluvastatin 78-89 sterol regulatory element binding transcription factor 1 Homo sapiens 94-101 30078674-7 2018 In this study, we examined the mechanism underlying cholesterol regulation by fluvastatin via SREBP-1 and AMPKalpha pathway and suggested that fluvastatin is an SIRT6 activator that regulates cholesterol homeostasis and fatty liver disease. Fluvastatin 78-89 sirtuin 6 Homo sapiens 161-166 30078674-7 2018 In this study, we examined the mechanism underlying cholesterol regulation by fluvastatin via SREBP-1 and AMPKalpha pathway and suggested that fluvastatin is an SIRT6 activator that regulates cholesterol homeostasis and fatty liver disease. Fluvastatin 143-154 sterol regulatory element binding transcription factor 1 Homo sapiens 94-101 30078674-7 2018 In this study, we examined the mechanism underlying cholesterol regulation by fluvastatin via SREBP-1 and AMPKalpha pathway and suggested that fluvastatin is an SIRT6 activator that regulates cholesterol homeostasis and fatty liver disease. Fluvastatin 143-154 sirtuin 6 Homo sapiens 161-166 30142209-10 2018 In SAMP6, BMP2, Runx2 and Bglap2 mRNA and protein expressions were significantly increased by fluvastatin, and ALP activity was increased by BMP2 action. Fluvastatin 94-105 runt related transcription factor 2 Mus musculus 16-21 30142209-10 2018 In SAMP6, BMP2, Runx2 and Bglap2 mRNA and protein expressions were significantly increased by fluvastatin, and ALP activity was increased by BMP2 action. Fluvastatin 94-105 bone gamma-carboxyglutamate protein 2 Mus musculus 26-32 30142209-11 2018 RhoA activity was also inhibited by fluvastatin. Fluvastatin 36-47 ras homolog family member A Mus musculus 0-4 30142209-12 2018 The concentration of fluvastatin sufficient to increase BMP2 and Runx2 expression and ALP activity was 0.5 muM in SAMP6 and 0.1 muM in SAMR1. Fluvastatin 21-32 bone morphogenetic protein 2 Mus musculus 56-60 30142209-12 2018 The concentration of fluvastatin sufficient to increase BMP2 and Runx2 expression and ALP activity was 0.5 muM in SAMP6 and 0.1 muM in SAMR1. Fluvastatin 21-32 runt related transcription factor 2 Mus musculus 65-70 30142209-13 2018 In conclusion, the present study revealed that fluvastatin promoted BMSC differentiation into osteoblasts by RhoA-BMP2 pathway in SAMP6. Fluvastatin 47-58 ras homolog family member A Mus musculus 109-113 30142209-13 2018 In conclusion, the present study revealed that fluvastatin promoted BMSC differentiation into osteoblasts by RhoA-BMP2 pathway in SAMP6. Fluvastatin 47-58 bone morphogenetic protein 2 Mus musculus 114-118 30116385-6 2018 After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Fluvastatin 6-17 toll-like receptor 4 Rattus norvegicus 106-110 30116385-6 2018 After fluvastatin treatment for 1 week, RT-qPCR found that compared with myocardial infarction group, the TLR4 mRNA expression of fluvastatin treatment group and normal control group was significantly increased, and the differences between groups were a statistically significant difference (P<0.05). Fluvastatin 130-141 toll-like receptor 4 Rattus norvegicus 106-110 30116385-7 2018 Western blot analysis showed that compared with the myocardial infarction group, the expression of TLR4 protein in normal control group, sham operation group and fluvastatin treatment group were significantly decreased, and they all were statistically significant (P<0.05). Fluvastatin 162-173 toll-like receptor 4 Rattus norvegicus 99-103 30116385-9 2018 Fluvastatin can inhibit myocardial infarction and decrease cardiomyocyte apoptosis by increasing the expression of TLR4-like receptor. Fluvastatin 0-11 toll-like receptor 4 Rattus norvegicus 115-119 29865262-6 2018 Simvastatin or fluvastatin caused IL-8 (interleukin-8) suppression, but increased hBD-2 mRNA expression in Salmonella-infected SW480 cells. Fluvastatin 15-26 C-X-C motif chemokine ligand 8 Homo sapiens 40-53 28744693-0 2018 VEGFA Involves in the Use of Fluvastatin and Zoledronate Against Breast Cancer. Fluvastatin 29-40 vascular endothelial growth factor A Homo sapiens 0-5 28744693-7 2018 VEGFA was up-regulated in both fluvastatin- and zoledronate-treated breast cancer cells. Fluvastatin 31-42 vascular endothelial growth factor A Homo sapiens 0-5 28744693-12 2018 Our results indicate that up-regulation of VEGFA may prevent the progression of breast cancer after fluvastatin and zoledronate treatment via inducing cell apoptosis and inhibiting migration and invasion. Fluvastatin 100-111 vascular endothelial growth factor A Homo sapiens 43-48 29865262-6 2018 Simvastatin or fluvastatin caused IL-8 (interleukin-8) suppression, but increased hBD-2 mRNA expression in Salmonella-infected SW480 cells. Fluvastatin 15-26 defensin beta 4A Homo sapiens 82-87 29520172-0 2018 Fluvastatin inhibits advanced glycation end products-induced proliferation, migration, and extracellular matrix accumulation in vascular smooth muscle cells by targeting connective tissue growth factor. Fluvastatin 0-11 cellular communication network factor 2 Homo sapiens 170-201 29373239-0 2018 Sorafenib and fluvastatin synergistically alleviate hepatic fibrosis via inhibiting the TGFbeta1/Smad3 pathway. Fluvastatin 14-25 transforming growth factor, beta 1 Rattus norvegicus 88-96 29373239-0 2018 Sorafenib and fluvastatin synergistically alleviate hepatic fibrosis via inhibiting the TGFbeta1/Smad3 pathway. Fluvastatin 14-25 SMAD family member 3 Rattus norvegicus 97-102 29373239-11 2018 Mechanistically, sorafenib plus fluvastatin blocked the TGFbeta1/Smad3 signaling pathway via inhibiting phosphorylation of TbetaR II in hepatocytes and HSCs. Fluvastatin 32-43 transforming growth factor, beta 1 Rattus norvegicus 56-64 29229608-6 2018 HRAS-induced epithelial-to-mesenchymal transition (EMT) through activation of zinc finger E-box binding homeobox 1 (ZEB1) sensitized tumor cells to the antiproliferative activity of statins, and induction of EMT by ZEB1 was sufficient to phenocopy the increase in fluvastatin sensitivity; knocking out ZEB1 reversed this effect. Fluvastatin 264-275 HRas proto-oncogene, GTPase Homo sapiens 0-4 29229608-6 2018 HRAS-induced epithelial-to-mesenchymal transition (EMT) through activation of zinc finger E-box binding homeobox 1 (ZEB1) sensitized tumor cells to the antiproliferative activity of statins, and induction of EMT by ZEB1 was sufficient to phenocopy the increase in fluvastatin sensitivity; knocking out ZEB1 reversed this effect. Fluvastatin 264-275 zinc finger E-box binding homeobox 1 Homo sapiens 78-114 29229608-6 2018 HRAS-induced epithelial-to-mesenchymal transition (EMT) through activation of zinc finger E-box binding homeobox 1 (ZEB1) sensitized tumor cells to the antiproliferative activity of statins, and induction of EMT by ZEB1 was sufficient to phenocopy the increase in fluvastatin sensitivity; knocking out ZEB1 reversed this effect. Fluvastatin 264-275 zinc finger E-box binding homeobox 1 Homo sapiens 116-120 29848699-5 2018 MLN8237 was combined with fluvastatin, an agent constraining nuclear localisation of YAP/TAZ for potential combination therapy in vitro. Fluvastatin 26-37 Yes1 associated transcriptional regulator Homo sapiens 85-88 29368187-2 2018 METHODS: The metabolism of diclofenac and fluvastatin in human recombinant CYP2C9 was investigated in the presence of EGCG. Fluvastatin 42-53 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 75-81 29373239-11 2018 Mechanistically, sorafenib plus fluvastatin blocked the TGFbeta1/Smad3 signaling pathway via inhibiting phosphorylation of TbetaR II in hepatocytes and HSCs. Fluvastatin 32-43 SMAD family member 3 Rattus norvegicus 65-70 29373239-11 2018 Mechanistically, sorafenib plus fluvastatin blocked the TGFbeta1/Smad3 signaling pathway via inhibiting phosphorylation of TbetaR II in hepatocytes and HSCs. Fluvastatin 32-43 transforming growth factor, beta receptor 2 Rattus norvegicus 123-132 29520172-7 2018 However, the inhibitory effect of fluvastatin was restored by administration of CTGF recombinant protein. Fluvastatin 34-45 cellular communication network factor 2 Homo sapiens 80-84 29520172-9 2018 Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Fluvastatin 0-11 cyclin D1 Homo sapiens 50-59 29520172-9 2018 Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Fluvastatin 0-11 cyclin dependent kinase 4 Homo sapiens 64-68 29520172-9 2018 Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Fluvastatin 0-11 interferon alpha inducible protein 27 Homo sapiens 118-121 29520172-9 2018 Fluvastatin repressed cell cycle regulatory genes cyclin D1 and Cdk4 and augmented cyclin-dependent kinase inhibitors p27 and p21 in AGE-induced VSMCs. Fluvastatin 0-11 cyclin dependent kinase inhibitor 1A Homo sapiens 126-129 29520172-10 2018 Taken together, fluvastatin suppressed AGE-induced VSMC proliferation, migration, and ECM accumulation by targeting CTGF signaling mechanism. Fluvastatin 16-27 cellular communication network factor 2 Homo sapiens 116-120 29445111-3 2018 Using Auditory Brainstem Responses (ABR) in a guinea pig model, we demonstrate that fluvastatin, an inhibitor of HMG-CoA reductase, the rate-limiting enzyme of the mevalonate pathway, protects against loss of cochlear function initiated by high intensity noise. Fluvastatin 84-95 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 113-130 29286128-0 2018 Protection against monocrotaline-induced pulmonary arterial hypertension and caveolin-1 downregulation by fluvastatin in rats. Fluvastatin 106-117 caveolin 1 Rattus norvegicus 77-87 29286128-4 2018 The present study was conducted to determine if fluvastatin was protective against experimental PAH development and to investigate the potential effects of fluvastatin on caveolin-1 (cav-1) expression. Fluvastatin 156-167 caveolin 1 Rattus norvegicus 171-181 29286128-4 2018 The present study was conducted to determine if fluvastatin was protective against experimental PAH development and to investigate the potential effects of fluvastatin on caveolin-1 (cav-1) expression. Fluvastatin 156-167 caveolin 1 Rattus norvegicus 183-188 29286128-11 2018 It was concluded that fluvastatin may protect against PAH development and ameliorate MCT induced inhibition of cav-1 expression in rats. Fluvastatin 22-33 caveolin 1 Rattus norvegicus 111-116 28005438-12 2018 On the other hand, gefitinib inhibited OATP1B1- and OATP2B1-mediated fluvastatin uptake. Fluvastatin 69-80 solute carrier organic anion transporter family member 1B1 Homo sapiens 39-46 29304533-9 2018 Fluvastatin and rosuvastatin interfered with MRP4 function inhibiting ATP-dependent cGMP (cyclic guanosine monophosphate) uptake into MRP4-containing vesicles, inhibited MRP4-mediated S1P transport in vitro and significantly attenuated endogenous S1P release from agonist-activated platelet ex vivo. Fluvastatin 0-11 ATP binding cassette subfamily C member 4 Homo sapiens 45-49 29304533-9 2018 Fluvastatin and rosuvastatin interfered with MRP4 function inhibiting ATP-dependent cGMP (cyclic guanosine monophosphate) uptake into MRP4-containing vesicles, inhibited MRP4-mediated S1P transport in vitro and significantly attenuated endogenous S1P release from agonist-activated platelet ex vivo. Fluvastatin 0-11 ATP binding cassette subfamily C member 4 Homo sapiens 134-138 29304533-9 2018 Fluvastatin and rosuvastatin interfered with MRP4 function inhibiting ATP-dependent cGMP (cyclic guanosine monophosphate) uptake into MRP4-containing vesicles, inhibited MRP4-mediated S1P transport in vitro and significantly attenuated endogenous S1P release from agonist-activated platelet ex vivo. Fluvastatin 0-11 ATP binding cassette subfamily C member 4 Homo sapiens 134-138 29304533-9 2018 Fluvastatin and rosuvastatin interfered with MRP4 function inhibiting ATP-dependent cGMP (cyclic guanosine monophosphate) uptake into MRP4-containing vesicles, inhibited MRP4-mediated S1P transport in vitro and significantly attenuated endogenous S1P release from agonist-activated platelet ex vivo. Fluvastatin 0-11 sphingosine-1-phosphate receptor 1 Mus musculus 184-187 29304533-9 2018 Fluvastatin and rosuvastatin interfered with MRP4 function inhibiting ATP-dependent cGMP (cyclic guanosine monophosphate) uptake into MRP4-containing vesicles, inhibited MRP4-mediated S1P transport in vitro and significantly attenuated endogenous S1P release from agonist-activated platelet ex vivo. Fluvastatin 0-11 sphingosine-1-phosphate receptor 1 Mus musculus 247-250 29670468-8 2018 Results: SAA-stimulated levels of released IL-6, IL-8, and sVCAM-1 from HCAEC were significantly attenuated by methotrexate, fluvastatin, and etoricoxib. Fluvastatin 125-136 serum amyloid A1 cluster Homo sapiens 9-12 29670468-8 2018 Results: SAA-stimulated levels of released IL-6, IL-8, and sVCAM-1 from HCAEC were significantly attenuated by methotrexate, fluvastatin, and etoricoxib. Fluvastatin 125-136 interleukin 6 Homo sapiens 43-47 29670468-8 2018 Results: SAA-stimulated levels of released IL-6, IL-8, and sVCAM-1 from HCAEC were significantly attenuated by methotrexate, fluvastatin, and etoricoxib. Fluvastatin 125-136 C-X-C motif chemokine ligand 8 Homo sapiens 49-53 29670468-11 2018 Conclusion: We observed marked influence of fluvastatin on lowering cytokine production in SAA-activated HCAEC. Fluvastatin 44-55 serum amyloid A1 cluster Homo sapiens 91-94 29375110-8 2018 Both pravastatin and fluvastatin significantly increased eNOS protein expression in ischemic and non-ischemic tissues compared to control. Fluvastatin 21-32 nitric oxide synthase 3 Rattus norvegicus 57-61 28005438-12 2018 On the other hand, gefitinib inhibited OATP1B1- and OATP2B1-mediated fluvastatin uptake. Fluvastatin 69-80 solute carrier organic anion transporter family member 2B1 Homo sapiens 52-59 29017950-8 2017 Downregulation of p53 occurred by VPA alone and fluvastatin alone, but not at their combined application; upregulation of p21 at the protein level was induced by each of the drugs alone and no further increase occurred at combined application. Fluvastatin 48-59 tumor protein p53 Homo sapiens 18-21 29212185-6 2017 Furthermore, treatment with fluvastatin, which regulates RHAMM transcription by modulating YAP1/TAZ activity, decreased the motility and invasion of MPM cells. Fluvastatin 28-39 hyaluronan mediated motility receptor Homo sapiens 57-62 29212185-6 2017 Furthermore, treatment with fluvastatin, which regulates RHAMM transcription by modulating YAP1/TAZ activity, decreased the motility and invasion of MPM cells. Fluvastatin 28-39 Yes1 associated transcriptional regulator Homo sapiens 91-95 28650504-1 2017 Fluvastatin (FLV) belongs to the group of compounds referred to as statins, also known as 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 90-147 28692940-0 2017 Betulinic acid and fluvastatin exhibits synergistic effect on toll-like receptor-4 mediated anti-atherogenic mechanism in type II collagen induced arthritis. Fluvastatin 19-30 toll like receptor 4 Homo sapiens 62-82 28692940-6 2017 Treatment with betulinic acid and fluvastatin showed significant (p<0.05) reduction in Arthritic index, Rheumatoid factor, C-reactive protein (CRP), total lipids and anti-CCP (cyclic citrullinated peptide) antibody. Fluvastatin 34-45 C-reactive protein Homo sapiens 126-144 28692940-6 2017 Treatment with betulinic acid and fluvastatin showed significant (p<0.05) reduction in Arthritic index, Rheumatoid factor, C-reactive protein (CRP), total lipids and anti-CCP (cyclic citrullinated peptide) antibody. Fluvastatin 34-45 C-reactive protein Homo sapiens 146-149 28883515-7 2017 Treatment with a specific FXa inhibitor, hydroxychloroquine or fluvastatin significantly reduced FXa-induced and IgG-potentiated Ca2+ release. Fluvastatin 63-74 coagulation factor X Homo sapiens 26-29 28883515-7 2017 Treatment with a specific FXa inhibitor, hydroxychloroquine or fluvastatin significantly reduced FXa-induced and IgG-potentiated Ca2+ release. Fluvastatin 63-74 coagulation factor X Homo sapiens 97-100 28511669-2 2017 We here test if the fasting levels of GH are cross-sectionally associated with carotid intima media thickness (IMT) and whether treatment with fluvastatin affects the fasting level of GH. Fluvastatin 143-154 growth hormone 1 Homo sapiens 184-186 28430117-12 2017 After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. Fluvastatin 110-121 C-reactive protein Homo sapiens 37-55 28430117-12 2017 After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. Fluvastatin 110-121 C-reactive protein Homo sapiens 57-60 28430117-13 2017 At 24 months of follow-up, CRP and HCY levels remained lower in the fluvastatin group than in the control group. Fluvastatin 68-79 C-reactive protein Homo sapiens 27-30 28542559-0 2017 Fluvastatin inhibits AGE-induced cell proliferation and migration via an ERK5-dependent Nrf2 pathway in vascular smooth muscle cells. Fluvastatin 0-11 mitogen-activated protein kinase 7 Homo sapiens 73-77 28542559-0 2017 Fluvastatin inhibits AGE-induced cell proliferation and migration via an ERK5-dependent Nrf2 pathway in vascular smooth muscle cells. Fluvastatin 0-11 NFE2 like bZIP transcription factor 2 Homo sapiens 88-92 28542559-6 2017 Furthermore, fluvastatin was found to significantly increase ARE promoter activity through ERK5 signaling, and to inhibit AGE-induced VSMC proliferation and migration as determined by MTT assay, cell counting, FACS analysis, a wound scratch assay, and a migration chamber assay. Fluvastatin 13-24 mitogen-activated protein kinase 7 Homo sapiens 91-95 28542559-8 2017 Moreover, fluvastatin suppressed the protein expressions of cyclin D1 and Cdk4, but induced p27, and blocked VSMC proliferation by regulating cell cycle. Fluvastatin 10-21 cyclin D1 Homo sapiens 60-69 28542559-8 2017 Moreover, fluvastatin suppressed the protein expressions of cyclin D1 and Cdk4, but induced p27, and blocked VSMC proliferation by regulating cell cycle. Fluvastatin 10-21 cyclin dependent kinase 4 Homo sapiens 74-78 28542559-8 2017 Moreover, fluvastatin suppressed the protein expressions of cyclin D1 and Cdk4, but induced p27, and blocked VSMC proliferation by regulating cell cycle. Fluvastatin 10-21 interferon alpha inducible protein 27 Homo sapiens 92-95 28430117-12 2017 After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. Fluvastatin 16-27 C-reactive protein Homo sapiens 37-55 28430117-12 2017 After 1 week of fluvastatin therapy, C-reactive protein (CRP) and homocysteine (HCY) levels were lower in the fluvastatin group than in the control group. Fluvastatin 16-27 C-reactive protein Homo sapiens 57-60 28302946-7 2017 Freezing time and 500 muM fluvastatin did not affect pore structures. Fluvastatin 26-37 latexin Homo sapiens 22-25 28500274-5 2017 We demonstrate that fluvastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic acid monohydrate, an inhibitor of protein prenylation, act synergistically to reverse outcomes of CCM3 loss in cultured mouse primary astrocytes and in Drosophila glial cells in vivo. Fluvastatin 20-31 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 49-96 28500274-5 2017 We demonstrate that fluvastatin, an inhibitor of 3-hydroxy-3-methyl-glutaryl (HMG)-CoA reductase and the N-bisphosphonate zoledronic acid monohydrate, an inhibitor of protein prenylation, act synergistically to reverse outcomes of CCM3 loss in cultured mouse primary astrocytes and in Drosophila glial cells in vivo. Fluvastatin 20-31 programmed cell death 10 Mus musculus 231-235 28511669-5 2017 Using multivariate linear regression models we related the change in GH-levels at 12 months compared with baseline to treatment with 40 mg fluvastatin once daily. Fluvastatin 139-150 growth hormone 1 Homo sapiens 69-71 28511669-8 2017 Treatment with fluvastatin was associated with a minor reduction in the fasting levels of hs-GH in males (p = 0.05) and a minor rise in the same levels among females (p = 0.05). Fluvastatin 15-26 growth hormone 1 Homo sapiens 93-95 28511669-10 2017 Treatment with fluvastatin for 12 months only had a minor, and probably not clinically relevant, effect on the fasting levels of hs-GH. Fluvastatin 15-26 growth hormone 1 Homo sapiens 132-134 28848611-7 2017 This study demonstrated that low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and triglycerides (TG) were reduced more with atorvastatin compared to simvastatin, pravastatin, lovastatin, and fluvastatin. Fluvastatin 211-222 component of oligomeric golgi complex 2 Homo sapiens 29-64 28454732-8 2017 Atg5 or Atg7 deletion, or 3-methyadenine (3-MA) or Bafilomycin A1 (Baf A1) treatment prevented the fluvastatin-induced suppression of bone metastasis. Fluvastatin 99-110 autophagy related 5 Mus musculus 0-4 28454732-8 2017 Atg5 or Atg7 deletion, or 3-methyadenine (3-MA) or Bafilomycin A1 (Baf A1) treatment prevented the fluvastatin-induced suppression of bone metastasis. Fluvastatin 99-110 autophagy related 7 Mus musculus 8-12 28454732-9 2017 Furthermore, we reveal that fluvastatin stimulation increased the nuclear p53 expression, and fluvastatin-induced autophagy and anti-bone metastatic activity were mostly dependent on p53. Fluvastatin 28-39 transformation related protein 53, pseudogene Mus musculus 74-77 28454732-9 2017 Furthermore, we reveal that fluvastatin stimulation increased the nuclear p53 expression, and fluvastatin-induced autophagy and anti-bone metastatic activity were mostly dependent on p53. Fluvastatin 94-105 transformation related protein 53, pseudogene Mus musculus 183-186 28457315-12 2017 TSP-1 plasma levels were increased in fluvastatin WT. Fluvastatin 38-49 thrombospondin 1 Mus musculus 0-5 28190756-6 2017 The OATP2B1-mediated theaflavin uptake was inhibited by known OATP2B1 substrates such as E3S, bromsulphthalein (BSP), dehydroepiandrosterone-3-sulfate (DHEAS), and fluvastatin. Fluvastatin 164-175 solute carrier organic anion transporter family member 2B1 Homo sapiens 4-11 28190756-6 2017 The OATP2B1-mediated theaflavin uptake was inhibited by known OATP2B1 substrates such as E3S, bromsulphthalein (BSP), dehydroepiandrosterone-3-sulfate (DHEAS), and fluvastatin. Fluvastatin 164-175 solute carrier organic anion transporter family member 2B1 Homo sapiens 62-69 28457315-13 2017 TSP-2 levels were decreased in fluvastatin WT and elevated in fluvastatin Thbs1-/-. Fluvastatin 31-42 tumor suppressor region 2 Mus musculus 0-5 28457315-13 2017 TSP-2 levels were decreased in fluvastatin WT and elevated in fluvastatin Thbs1-/-. Fluvastatin 62-73 tumor suppressor region 2 Mus musculus 0-5 28457315-13 2017 TSP-2 levels were decreased in fluvastatin WT and elevated in fluvastatin Thbs1-/-. Fluvastatin 62-73 thrombospondin 1 Mus musculus 74-79 26935883-8 2016 MCT4 knockdown suppressed atorvastatin-, simvastatin-, and fluvastatin-induced reduction of cell viability and apoptosis compared with negative control-treated cells. Fluvastatin 59-70 solute carrier family 16 member 3 Homo sapiens 0-4 28674251-0 2017 Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants. Fluvastatin 21-32 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 122-128 28674251-0 2017 Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants. Fluvastatin 95-106 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 37-43 28674251-0 2017 Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants. Fluvastatin 95-106 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 48-54 28674251-0 2017 Co-administration of Fluvastatin and CYP3A4 and CYP2C8 Inhibitors May Increase the Exposure to Fluvastatin in Carriers of CYP2C9 Genetic Variants. Fluvastatin 95-106 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 122-128 28674251-1 2017 Fluvastatin, which is one of the hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins), is primarily metabolized by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-1 2017 Fluvastatin, which is one of the hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins), is primarily metabolized by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8. Fluvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 162-168 28674251-1 2017 Fluvastatin, which is one of the hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitors (statins), is primarily metabolized by CYP2C9 and to a lesser extent by CYP3A4 and CYP2C8. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 173-179 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 6-12 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 76-82 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-90 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 96-102 28674251-4 2017 Since CYP2C9 is a polymorphic enzyme, we investigated the effect of DDI via CYP2C9, CYP3A4, and CYP2C8 on fluvastatin pharmacokinetics by using a validated prediction method in relation to CYP2C9 variants. Fluvastatin 106-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 76-82 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 116-122 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-5 2017 The predicted increases in the area under the concentration-time curve (AUC) ratios of fluvastatin in carriers with CYP2C9*1/*2, CYP2C9*1/*3, CYP2C9*2/*2, CYP2C9*2/*3, and CYP2C9*3/*3 versus that found in carriers with CYP2C9*1/*1 were 1.16, 1.35, 1.37, 1.65, and 2.06, respectively. Fluvastatin 87-98 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 53-64 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 53-64 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 144-150 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 53-64 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 172-178 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 53-64 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 316-322 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 335-346 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 133-139 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 335-346 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 144-150 28674251-6 2017 Our in silico model predicted that administration of fluvastatin in conjunction with the potent inhibitors that completely inhibited CYP3A4 and CYP2C8 in carriers with the CYP2C9*3/*3 variant would cause a 3.23- and 2.60-fold increase in the AUC ratios, respectively, when compared to that for the carriers with the CYP2C9*1/*1 taking fluvastatin alone. Fluvastatin 335-346 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 172-178 28214901-0 2017 Protective Effects of Fluvastatin on Reproductive Function in Obese Male Rats Induced by High-Fat Diet through Enhanced Signaling of mTOR. Fluvastatin 22-33 mechanistic target of rapamycin kinase Rattus norvegicus 133-137 28214901-10 2017 Fluvastatin also partially reversed the suppression of mTOR and p-p70s6k expresson. Fluvastatin 0-11 mechanistic target of rapamycin kinase Rattus norvegicus 55-59 28214901-10 2017 Fluvastatin also partially reversed the suppression of mTOR and p-p70s6k expresson. Fluvastatin 0-11 ribosomal protein S6 kinase B1 Rattus norvegicus 66-72 28214901-11 2017 CONCLUSION: Our data suggest that fluvastatin has protective effects on reproductive function in obese male rats most probably through enhanced signaling of mTOR. Fluvastatin 34-45 mechanistic target of rapamycin kinase Rattus norvegicus 157-161 27102210-5 2016 CONCLUSION: These results indicate that fluvastatin increases in adenosine concentrations in the dialysate which resulted from activation of PKC, mediated by stimulation of alpha1-adrenoceptors, through activation of ecto-5"-nucleotidase. Fluvastatin 40-51 5' nucleotidase, ecto Rattus norvegicus 217-237 27858552-6 2017 RESULTS: Fluvastatin significantly inhibited both RANKL- and LPS-induced osteoclast differentiation in mouse BMMs. Fluvastatin 9-20 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 50-55 27858552-7 2017 Fluvastatin also markedly reduced expression of osteoclast differentiation marker genes Acp5, Calcr, and Ctsk as well as fusion markers Atp6v0d2 and Dcstamp. Fluvastatin 0-11 acid phosphatase 5, tartrate resistant Mus musculus 88-92 27858552-7 2017 Fluvastatin also markedly reduced expression of osteoclast differentiation marker genes Acp5, Calcr, and Ctsk as well as fusion markers Atp6v0d2 and Dcstamp. Fluvastatin 0-11 calcitonin receptor Mus musculus 94-99 27858552-7 2017 Fluvastatin also markedly reduced expression of osteoclast differentiation marker genes Acp5, Calcr, and Ctsk as well as fusion markers Atp6v0d2 and Dcstamp. Fluvastatin 0-11 cathepsin K Mus musculus 105-109 27858552-7 2017 Fluvastatin also markedly reduced expression of osteoclast differentiation marker genes Acp5, Calcr, and Ctsk as well as fusion markers Atp6v0d2 and Dcstamp. Fluvastatin 0-11 ATPase, H+ transporting, lysosomal V0 subunit D2 Mus musculus 136-144 27858552-7 2017 Fluvastatin also markedly reduced expression of osteoclast differentiation marker genes Acp5, Calcr, and Ctsk as well as fusion markers Atp6v0d2 and Dcstamp. Fluvastatin 0-11 dendrocyte expressed seven transmembrane protein Mus musculus 149-156 27858552-9 2017 Fluvastatin reduced generation of reactive oxygen species upon the addition of RANKL and LPS, suggesting an antioxidant role. Fluvastatin 0-11 tumor necrosis factor (ligand) superfamily, member 11 Mus musculus 79-84 28089347-6 2017 Our results demonstrated that statin compounds Pitavastatin (1) and Fluvastatin (4) could bind to the LBP of RXRalpha (KD=13.30muM and 11.04muM, respectively) and serve as transcriptional antagonists of RXRalpha. Fluvastatin 68-79 lipopolysaccharide binding protein Homo sapiens 102-105 28089347-6 2017 Our results demonstrated that statin compounds Pitavastatin (1) and Fluvastatin (4) could bind to the LBP of RXRalpha (KD=13.30muM and 11.04muM, respectively) and serve as transcriptional antagonists of RXRalpha. Fluvastatin 68-79 retinoid X receptor alpha Homo sapiens 109-117 28089347-6 2017 Our results demonstrated that statin compounds Pitavastatin (1) and Fluvastatin (4) could bind to the LBP of RXRalpha (KD=13.30muM and 11.04muM, respectively) and serve as transcriptional antagonists of RXRalpha. Fluvastatin 68-79 retinoid X receptor alpha Homo sapiens 203-211 28478461-9 2017 Flu decreased atherosclerotic plaque, calcium deposition, lipid cores, intraplaque hemorrhage, erythrocyte membranes, endothelial cells, and macrophage infiltration, while increasing smooth muscle cells in plaques of both aortic segments; it also lowered TLR2, 3, 4, and 8 expression in all aortic segments to a stronger degree than resumption of normal diet. Fluvastatin 0-3 toll-like receptor 2 Oryctolagus cuniculus 255-262 27734263-11 2016 Simvastatin and fluvastatin showed very strong growth suppressive effects, and induced apoptosis in HLF cells, but not HuH1 cells. Fluvastatin 16-27 HLF transcription factor, PAR bZIP family member Homo sapiens 100-103 27734263-12 2016 TAZ expression was suppressed in HLF cells by fluvastatin and simvastatin treatment. Fluvastatin 46-57 tafazzin, phospholipid-lysophospholipid transacylase Homo sapiens 0-3 27734263-12 2016 TAZ expression was suppressed in HLF cells by fluvastatin and simvastatin treatment. Fluvastatin 46-57 HLF transcription factor, PAR bZIP family member Homo sapiens 33-36 26899523-0 2016 A Clinical Study Evaluating the Effects of Fluvastatin on Serum Osteoprotegerin Levels in Rheumatoid Arthritis Patients. Fluvastatin 43-54 TNF receptor superfamily member 11b Homo sapiens 64-79 26899523-6 2016 After 12 weeks, the OPG level was significantly increased in the fluvastatin group compared to the placebo group. Fluvastatin 65-76 TNF receptor superfamily member 11b Homo sapiens 20-23 26899523-9 2016 In conclusion, fluvastatin administration could increase the OPG levels and improve disease activity variables in patients with RA. Fluvastatin 15-26 TNF receptor superfamily member 11b Homo sapiens 61-64 27181081-6 2016 Furthermore, we aimed to determine the effect of ZOL and FLU combination on RhoA and Ras guanosine 5"-triphosphate (GTP)-proteins. Fluvastatin 57-60 ras homolog family member A Homo sapiens 76-80 27173404-6 2016 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor fluvastatin could also be shown to moderately reduce the IL-33-mediated effect on M-CSF, but not on GM-CSF expression. Fluvastatin 72-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-61 27173404-6 2016 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor fluvastatin could also be shown to moderately reduce the IL-33-mediated effect on M-CSF, but not on GM-CSF expression. Fluvastatin 72-83 interleukin 33 Homo sapiens 129-134 27173404-6 2016 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor fluvastatin could also be shown to moderately reduce the IL-33-mediated effect on M-CSF, but not on GM-CSF expression. Fluvastatin 72-83 colony stimulating factor 1 Homo sapiens 154-159 27173404-6 2016 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor fluvastatin could also be shown to moderately reduce the IL-33-mediated effect on M-CSF, but not on GM-CSF expression. Fluvastatin 72-83 colony stimulating factor 2 Homo sapiens 172-178 26419593-0 2016 Antimetastatic effect of fluvastatin on breast and hepatocellular carcinoma cells in relation to SGK1 and NDRG1 genes. Fluvastatin 25-36 serum/glucocorticoid regulated kinase 1 Homo sapiens 97-101 26419593-0 2016 Antimetastatic effect of fluvastatin on breast and hepatocellular carcinoma cells in relation to SGK1 and NDRG1 genes. Fluvastatin 25-36 N-myc downstream regulated 1 Homo sapiens 106-111 26419593-7 2016 Consequently, fluvastatin dose-dependently inhibited migration induced by TGF-beta1 in both groups. Fluvastatin 14-25 transforming growth factor beta 1 Homo sapiens 74-83 26093510-7 2015 Fluvastatin (AUC50=12.5 +- 1.2 muM) and enalapril (AUC50=15.2 +- 1.8 muM) showed high ability to prevent myoglobin peroxidation, providing even better efficiency than endogenous antioxidants such as reduced glutathione. Fluvastatin 0-11 latexin Homo sapiens 31-34 26832408-4 2016 We explored two hits: the MEK inhibitor trametinib and the HMG-CoA reductase inhibitor fluvastatin. Fluvastatin 87-98 HMG Coenzyme A reductase Drosophila melanogaster 59-76 26832408-5 2016 Oral administration of these drugs inhibited Ras and PI3K pathway activity, respectively; in addition, fluvastatin inhibited protein prenylation downstream of HMG-CoA reductase to promote survival. Fluvastatin 103-114 HMG Coenzyme A reductase Drosophila melanogaster 159-176 26773154-7 2016 Fluvastatin selectively suppressed key FcepsilonRI signaling pathways, including Akt and ERK. Fluvastatin 0-11 thymoma viral proto-oncogene 1 Mus musculus 81-84 26773154-7 2016 Fluvastatin selectively suppressed key FcepsilonRI signaling pathways, including Akt and ERK. Fluvastatin 0-11 mitogen-activated protein kinase 1 Mus musculus 89-92 26863535-0 2016 Simvastatin Sodium Salt and Fluvastatin Interact with Human Gap Junction Gamma-3 Protein. Fluvastatin 28-39 gap junction protein gamma 3 Homo sapiens 60-88 25858254-9 2016 They also inhibited OATP-mediated uptake of atorvastatin, fluvastatin, and rosuvastatin. Fluvastatin 58-69 solute carrier organic anion transporter family member 1A2 Homo sapiens 20-24 26707305-13 2015 Further placebo-controlled treatment studies would be helpful to evaluate the effects of fluvastatin on oxidant and antioxidant parameters including PON1 in patients with KT. Fluvastatin 89-100 paraoxonase 1 Homo sapiens 149-153 26093510-7 2015 Fluvastatin (AUC50=12.5 +- 1.2 muM) and enalapril (AUC50=15.2 +- 1.8 muM) showed high ability to prevent myoglobin peroxidation, providing even better efficiency than endogenous antioxidants such as reduced glutathione. Fluvastatin 0-11 latexin Homo sapiens 69-72 26093510-7 2015 Fluvastatin (AUC50=12.5 +- 1.2 muM) and enalapril (AUC50=15.2 +- 1.8 muM) showed high ability to prevent myoglobin peroxidation, providing even better efficiency than endogenous antioxidants such as reduced glutathione. Fluvastatin 0-11 myoglobin Homo sapiens 105-114 26093510-8 2015 Moreover, labetalol, enalapril and fluvastatin prevent the autoxidation of myoglobin, while glutathione showed a pro-oxidant effect. Fluvastatin 35-46 myoglobin Homo sapiens 75-84 26353928-6 2015 SREBP2 knockdown in lung and breast cancer cells completely abrogated the fluvastatin-induced upregulation of sterol-responsive genes HMGCR and HMGCS1. Fluvastatin 74-85 sterol regulatory element binding transcription factor 2 Homo sapiens 0-6 26353928-6 2015 SREBP2 knockdown in lung and breast cancer cells completely abrogated the fluvastatin-induced upregulation of sterol-responsive genes HMGCR and HMGCS1. Fluvastatin 74-85 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 134-139 26353928-6 2015 SREBP2 knockdown in lung and breast cancer cells completely abrogated the fluvastatin-induced upregulation of sterol-responsive genes HMGCR and HMGCS1. Fluvastatin 74-85 3-hydroxy-3-methylglutaryl-CoA synthase 1 Homo sapiens 144-150 26353928-7 2015 Knockdown of SREBP2 alone did not affect three-dimensional growth of lung and breast cancer cells, yet in combination with fluvastatin cell growth was disrupted. Fluvastatin 123-134 sterol regulatory element binding transcription factor 2 Homo sapiens 13-19 26070251-9 2015 Furthermore, the expression of the efflux transporter P-gp was increased in fluvastatin-resistant replicon cells (determined by qRT-PCR and flow cytometry). Fluvastatin 76-87 phosphoglycolate phosphatase Homo sapiens 54-58 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 nuclear receptor subfamily 1 group I member 2 Homo sapiens 91-110 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 nuclear receptor subfamily 1 group I member 2 Homo sapiens 111-114 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 126-132 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 134-140 26366873-0 2015 Optical Isomers of Atorvastatin, Rosuvastatin and Fluvastatin Enantiospecifically Activate Pregnane X Receptor PXR and Induce CYP2A6, CYP2B6 and CYP3A4 in Human Hepatocytes. Fluvastatin 50-61 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 145-151 26366873-8 2015 Basal transcriptional activity of GR was not affected by tested statins, but dexamethasone-inducible activity of GR was dose-dependently and enantioselectively inhibited by fluvastatin. Fluvastatin 173-184 nuclear receptor subfamily 3 group C member 1 Homo sapiens 34-36 26366873-8 2015 Basal transcriptional activity of GR was not affected by tested statins, but dexamethasone-inducible activity of GR was dose-dependently and enantioselectively inhibited by fluvastatin. Fluvastatin 173-184 nuclear receptor subfamily 3 group C member 1 Homo sapiens 113-115 26622466-12 2015 Combining these findings, cyclic intermittent treatment with a low-dose fluvastatin and valsartan combination is proposed as a new cardiovascular preventive strategy in patients with DM1. Fluvastatin 72-83 immunoglobulin heavy diversity 1-7 Homo sapiens 183-186 25886887-9 2015 RESULTS: In vitro, Flu (1-20 muM) inhibited PA-induced free-radical production, gp91 (phox) expression, and NFkappaB p65 translocation in HepG2 and PRHs, while CM-induced alpha-SMA protein expression and pro-fibrogenic gene expressions in HSC-T6 were suppressed in Flu-pretreated cells compared to those without pretreatment. Fluvastatin 19-22 synaptotagmin 1 Rattus norvegicus 117-120 25735397-0 2015 Fluvastatin Upregulates the Expression of Tissue Factor Pathway Inhibitor in Human Umbilical Vein Endothelial Cells. Fluvastatin 0-11 tissue factor pathway inhibitor Homo sapiens 42-73 25735397-3 2015 We investigated the effect of fluvastatin on TFPI expression in cultured endothelial cells. Fluvastatin 30-41 tissue factor pathway inhibitor Homo sapiens 45-49 25735397-7 2015 A luciferase reporter assay was performed to evaluate the effect of fluvastatin on TFPI transcription. Fluvastatin 68-79 tissue factor pathway inhibitor Homo sapiens 83-87 25735397-9 2015 RESULTS: Fluvastatin increased TFPI mRNA expression and antigen in HUVECs. Fluvastatin 9-20 tissue factor pathway inhibitor Homo sapiens 31-35 25735397-10 2015 Fluvastatin-induced TFPI expression was reversed by co-treatment with mevalonate or geranylgeranylpyrophosphate (GGPP). Fluvastatin 0-11 tissue factor pathway inhibitor Homo sapiens 20-24 25735397-12 2015 SB203580, GF109203, and LY294002 reduced fluvastatin-induced TFPI upregulation. Fluvastatin 41-52 tissue factor pathway inhibitor Homo sapiens 61-65 24942605-12 2015 Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF. Fluvastatin 13-24 serum/glucocorticoid regulated kinase 1 Homo sapiens 76-80 24942605-12 2015 Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF. Fluvastatin 13-24 fibronectin 1 Homo sapiens 85-87 24942605-12 2015 Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF. Fluvastatin 13-24 serum/glucocorticoid regulated kinase 1 Homo sapiens 76-80 24942605-12 2015 Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF. Fluvastatin 13-24 serum/glucocorticoid regulated kinase 1 Homo sapiens 76-80 24942605-12 2015 Treated with fluvastatin and the SGK1-inhibitor GSK650394, abnormalities of SGK1 and FN could be corrected partially, which suggested that the SGK1 pathway was implicated in the pathogenesis of PF, and that fluvastatin might decrease the expression of SGK1 so as to meliorate the progression of PF. Fluvastatin 207-218 serum/glucocorticoid regulated kinase 1 Homo sapiens 33-37 25380981-2 2015 METHODS: The correlation of the changes of the area under the plasma concentration-time curve (AUC) caused by ABCG2 421C>A with those caused by the Bcrp knockout in mice, or BCRP inhibition in monkeys, was investigated using well-known BCRP substrates (rosuvastatin, pitavastatin, fluvastatin, and sulfasalazine). Fluvastatin 284-295 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 110-115 25735397-14 2015 TFPI mRNA degradation in the presence of actinomycin D was delayed by fluvastatin treatment. Fluvastatin 70-81 tissue factor pathway inhibitor Homo sapiens 0-4 25735397-15 2015 CONCLUSIONS: Fluvastatin increases endothelial TFPI expression through inhibition of mevalonate-, GGPP-, and Cdc42-dependent signaling pathways, and activation of the p38 MAPK, PI3K, and PKC pathways. Fluvastatin 13-24 tissue factor pathway inhibitor Homo sapiens 47-51 25735397-15 2015 CONCLUSIONS: Fluvastatin increases endothelial TFPI expression through inhibition of mevalonate-, GGPP-, and Cdc42-dependent signaling pathways, and activation of the p38 MAPK, PI3K, and PKC pathways. Fluvastatin 13-24 cell division cycle 42 Homo sapiens 109-114 24942605-0 2015 Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway. Fluvastatin 0-11 fibronectin 1 Homo sapiens 39-50 24942605-0 2015 Fluvastatin inhibits the expression of fibronectin in human peritoneal mesothelial cells induced by high-glucose peritoneal dialysis solution via SGK1 pathway. Fluvastatin 0-11 serum/glucocorticoid regulated kinase 1 Homo sapiens 146-150 24942605-6 2015 The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway. Fluvastatin 50-61 fibronectin 1 Homo sapiens 93-104 24942605-6 2015 The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway. Fluvastatin 50-61 fibronectin 1 Homo sapiens 106-108 24942605-6 2015 The purpose of this study was to identify whether fluvastatin may decrease the expression of fibronectin (FN) in human peritoneal mesothelial cells (HPMC) cultured with high-glucose peritoneal dialysis solution (HGPDS) by affecting SGK1 signal pathway. Fluvastatin 50-61 serum/glucocorticoid regulated kinase 1 Homo sapiens 232-236 25529449-6 2015 Fluvastatin and pitavastatin activated PPARgamma in HASMCs, but not in HUVECs. Fluvastatin 0-11 peroxisome proliferator activated receptor gamma Homo sapiens 39-48 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 BCL2 associated X, apoptosis regulator Homo sapiens 136-139 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 BCL2 apoptosis regulator Homo sapiens 140-145 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 cytochrome c, somatic Homo sapiens 163-175 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 caspase 9 Homo sapiens 196-205 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 caspase 3 Homo sapiens 210-219 25434456-8 2015 Subsequent studies confirmed the results of array and demonstrated that fluvastatin activated mitochondrial apoptosis through enhancing bax/bcl-2 ratio, releasing cytochrome c, in turn activating caspase-9 and caspase-3, and eventually cleaving PARP. Fluvastatin 72-83 collagen type XI alpha 2 chain Homo sapiens 245-249 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 insulin like growth factor binding protein 6 Homo sapiens 109-116 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 interferon alpha inducible protein 27 Homo sapiens 118-121 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 tumor protein p53 Homo sapiens 123-126 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 cyclin B1 Homo sapiens 156-165 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 cyclin D1 Homo sapiens 167-176 25434456-9 2015 Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression. Fluvastatin 68-79 vascular endothelial growth factor A Homo sapiens 181-185 25347557-0 2014 Cytotoxic effect of fluvastatin on MCF-7 cells possibly through a reduction of the mRNA expression levels of SGK1 and CAV1. Fluvastatin 20-31 caveolin 1 Homo sapiens 118-122 26058399-6 2015 Fluvastatin is metabolized by CYP2C9, while pravastatin, rosuvastatin and pitavastatin are not susceptible to inhibition by any CYP. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 30-36 25240415-0 2015 Fluvastatin attenuated the effect of expression of beta1 integrin in PAN-treated podocytes by inhibiting reactive oxygen species. Fluvastatin 0-11 integrin subunit beta 1 Homo sapiens 51-65 25240415-3 2015 In the present study, we investigated the effect and mechanism of fluvastatin (FLV) on the expression of beta1 integrin in puromycin aminonucleoside (PAN)-treated podocytes in vitro. Fluvastatin 66-77 integrin subunit beta 1 Homo sapiens 105-119 25240415-3 2015 In the present study, we investigated the effect and mechanism of fluvastatin (FLV) on the expression of beta1 integrin in puromycin aminonucleoside (PAN)-treated podocytes in vitro. Fluvastatin 79-82 integrin subunit beta 1 Homo sapiens 105-119 25379722-7 2015 Restricting the analysis to patients receiving simvastatin, pravastatin, lovastatin and fluvastatin indicated a statistically significant association of the OATP1B1 genotype on lipid parameters at the 5-year follow-up. Fluvastatin 88-99 solute carrier organic anion transporter family member 1B1 Homo sapiens 157-164 24917577-0 2014 Fluvastatin causes NLRP3 inflammasome-mediated adipose insulin resistance. Fluvastatin 0-11 NLR family, pyrin domain containing 3 Mus musculus 19-24 24917577-7 2014 Fluvastatin-induced activation of the NLRP3/caspase-1 pathway was required for the development of insulin resistance in adipose tissue explants, an effect also prevented by glyburide. Fluvastatin 0-11 NLR family, pyrin domain containing 3 Mus musculus 38-43 24917577-7 2014 Fluvastatin-induced activation of the NLRP3/caspase-1 pathway was required for the development of insulin resistance in adipose tissue explants, an effect also prevented by glyburide. Fluvastatin 0-11 caspase 1 Mus musculus 44-53 24917577-8 2014 Fluvastatin impaired insulin signaling in lipopolysaccharide-primed 3T3-L1 adipocytes, an effect associated with increased caspase-1 activity, but not IL-1beta secretion. Fluvastatin 0-11 caspase 1 Mus musculus 123-132 25347557-0 2014 Cytotoxic effect of fluvastatin on MCF-7 cells possibly through a reduction of the mRNA expression levels of SGK1 and CAV1. Fluvastatin 20-31 serum/glucocorticoid regulated kinase 1 Homo sapiens 109-113 25347557-11 2014 The antiproliferative effects of FLU may be related to the decreased expression levels of SGK1 and CAV1. Fluvastatin 33-36 serum/glucocorticoid regulated kinase 1 Homo sapiens 90-94 25347557-11 2014 The antiproliferative effects of FLU may be related to the decreased expression levels of SGK1 and CAV1. Fluvastatin 33-36 caveolin 1 Homo sapiens 99-103 25280537-0 2014 Creatine kinase elevation caused by a combination of fluvastatin and telmisartan in a patient heterozygous for the CYP2C9*3 and ABCC2 -24C > T variants: a case report. Fluvastatin 53-64 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 115-121 25280537-0 2014 Creatine kinase elevation caused by a combination of fluvastatin and telmisartan in a patient heterozygous for the CYP2C9*3 and ABCC2 -24C > T variants: a case report. Fluvastatin 53-64 ATP binding cassette subfamily C member 2 Homo sapiens 128-133 24976507-11 2014 By combining archazolid B with the HMGCR inhibitor fluvastatin, cholesterol was reduced and cell viability decreased by about 20% compared to archazolid B treatment alone. Fluvastatin 51-62 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 35-40 25268751-6 2014 Fluvastatin treatment caused proteolysis of vimentin, a marker of epithelial to mesenchymal transition. Fluvastatin 0-11 vimentin Homo sapiens 44-52 25268751-7 2014 This effect of fluvastatin was reversed in the presence of mevalonate, a downstream product of HMG-CoA and caspase-3 inhibitor. Fluvastatin 15-26 caspase 3 Homo sapiens 107-116 25268751-8 2014 Interestingly, fluvastatin neither caused an appreciable cell death nor did modulate vimentin expression in normal mammary epithelial cells. Fluvastatin 15-26 vimentin Homo sapiens 85-93 25268751-9 2014 In conclusion, fluvastatin alters levels of cytoskeletal proteins, primarily targeting vimentin through increased caspase-3- mediated proteolysis, thereby suggesting a role for vimentin in statin-induced breast cancer cell death. Fluvastatin 15-26 vimentin Homo sapiens 87-95 25268751-9 2014 In conclusion, fluvastatin alters levels of cytoskeletal proteins, primarily targeting vimentin through increased caspase-3- mediated proteolysis, thereby suggesting a role for vimentin in statin-induced breast cancer cell death. Fluvastatin 15-26 caspase 3 Homo sapiens 114-123 25268751-9 2014 In conclusion, fluvastatin alters levels of cytoskeletal proteins, primarily targeting vimentin through increased caspase-3- mediated proteolysis, thereby suggesting a role for vimentin in statin-induced breast cancer cell death. Fluvastatin 15-26 vimentin Homo sapiens 177-185 24964743-9 2014 Notably, fluvastatin increased manganese superoxide dismutase (by repressing the transcription factor DNA damage-binding protein 2), catalase and glutathione which, in turn, diminished H2 O2 levels. Fluvastatin 9-20 damage specific DNA binding protein 2 Homo sapiens 102-130 24964743-5 2014 Interestingly, fluvastatin downregulated transferrin receptor (TfR1), with a concomitant depletion of intracellular iron levels in these cells. Fluvastatin 15-26 transferrin receptor Homo sapiens 63-67 24951966-7 2014 Moreover, fluvastatin and atorvastatin enhanced the mRNA and protein expression of cystathionine gamma-lyase (CSE) in dose- and time-dependent manners. Fluvastatin 10-21 cystathionine gamma-lyase Homo sapiens 83-108 24951966-7 2014 Moreover, fluvastatin and atorvastatin enhanced the mRNA and protein expression of cystathionine gamma-lyase (CSE) in dose- and time-dependent manners. Fluvastatin 10-21 cystathionine gamma-lyase Homo sapiens 110-113 24951966-8 2014 Fluvastatin also markedly enhanced the CSE activity. Fluvastatin 0-11 cystathionine gamma-lyase Homo sapiens 39-42 24951966-10 2014 Blockade of CSE with its inhibitor dl-propargylglycine (PAG) or siRNA markedly reduced the H2S level in fluvastatin-stimulated macrophages. Fluvastatin 104-115 cystathionine gamma-lyase Homo sapiens 12-15 24951966-11 2014 In addition, fluvastatin elevated Akt phosphorylation, which occurred as early as 15 min after treatment, peaked at 1h, and lasted at least 3h. Fluvastatin 13-24 AKT serine/threonine kinase 1 Homo sapiens 34-37 24951966-12 2014 Both PI3K inhibitor LY294002 (10 muM) and Akt inhibitor perifosine (10muM) were able to reverse the increases of CSE mRNA and H2S production in fluvastatin-stimulated macrophages. Fluvastatin 144-155 latexin Homo sapiens 33-36 24951966-12 2014 Both PI3K inhibitor LY294002 (10 muM) and Akt inhibitor perifosine (10muM) were able to reverse the increases of CSE mRNA and H2S production in fluvastatin-stimulated macrophages. Fluvastatin 144-155 AKT serine/threonine kinase 1 Homo sapiens 42-45 24951966-12 2014 Both PI3K inhibitor LY294002 (10 muM) and Akt inhibitor perifosine (10muM) were able to reverse the increases of CSE mRNA and H2S production in fluvastatin-stimulated macrophages. Fluvastatin 144-155 cystathionine gamma-lyase Homo sapiens 113-116 24951966-13 2014 Last, we showed that fluvastatin reduced the mRNA levels of pro-inflammatory molecules such as IL-1beta and MCP-1 in LPS-treated macrophages, which were completely reversed by CSE inhibitor PAG. Fluvastatin 21-32 interleukin 1 beta Homo sapiens 95-103 24951966-13 2014 Last, we showed that fluvastatin reduced the mRNA levels of pro-inflammatory molecules such as IL-1beta and MCP-1 in LPS-treated macrophages, which were completely reversed by CSE inhibitor PAG. Fluvastatin 21-32 C-C motif chemokine ligand 2 Homo sapiens 108-113 24951966-13 2014 Last, we showed that fluvastatin reduced the mRNA levels of pro-inflammatory molecules such as IL-1beta and MCP-1 in LPS-treated macrophages, which were completely reversed by CSE inhibitor PAG. Fluvastatin 21-32 cystathionine gamma-lyase Homo sapiens 176-179 24964743-9 2014 Notably, fluvastatin increased manganese superoxide dismutase (by repressing the transcription factor DNA damage-binding protein 2), catalase and glutathione which, in turn, diminished H2 O2 levels. Fluvastatin 9-20 catalase Homo sapiens 133-141 24964743-10 2014 Fluvastatin-induced downregulation of TfR1, matrix metalloproteinase-2, -9 and inhibition of invasion were reversed in the presence of aminotriazole, a specific inhibitor of catalase. Fluvastatin 0-11 transferrin receptor Homo sapiens 38-42 24964743-10 2014 Fluvastatin-induced downregulation of TfR1, matrix metalloproteinase-2, -9 and inhibition of invasion were reversed in the presence of aminotriazole, a specific inhibitor of catalase. Fluvastatin 0-11 matrix metallopeptidase 2 Homo sapiens 44-74 24964743-10 2014 Fluvastatin-induced downregulation of TfR1, matrix metalloproteinase-2, -9 and inhibition of invasion were reversed in the presence of aminotriazole, a specific inhibitor of catalase. Fluvastatin 0-11 catalase Homo sapiens 174-182 23979266-8 2014 Fluvastatin enhanced myocardial endothelial nitric oxide synthase (eNOS) protein levels and increased eNOS, vascular endothelial growth factor, and hypoxia-inducible factor-1alpha mRNA expression. Fluvastatin 0-11 hypoxia inducible factor 1 subunit alpha Rattus norvegicus 108-179 24522493-7 2014 Since we previously reported that fluvastatin treatment increased AQP2 plasma membrane expression in wild-type mice, secretin-infused X-NDI mice received a single injection of fluvastatin. Fluvastatin 34-45 aquaporin 2 Mus musculus 66-70 23979266-7 2014 Myocardial oxidative stress increased in DM, but fluvastatin significantly reduced p22(phox) and gp91(phox) mRNA expression and myocardial PGF(2alpha) levels. Fluvastatin 49-60 cytochrome b-245 alpha chain Rattus norvegicus 87-91 23979266-7 2014 Myocardial oxidative stress increased in DM, but fluvastatin significantly reduced p22(phox) and gp91(phox) mRNA expression and myocardial PGF(2alpha) levels. Fluvastatin 49-60 cytochrome b-245 alpha chain Rattus norvegicus 102-106 23979266-8 2014 Fluvastatin enhanced myocardial endothelial nitric oxide synthase (eNOS) protein levels and increased eNOS, vascular endothelial growth factor, and hypoxia-inducible factor-1alpha mRNA expression. Fluvastatin 0-11 nitric oxide synthase 3 Rattus norvegicus 32-65 23979266-8 2014 Fluvastatin enhanced myocardial endothelial nitric oxide synthase (eNOS) protein levels and increased eNOS, vascular endothelial growth factor, and hypoxia-inducible factor-1alpha mRNA expression. Fluvastatin 0-11 nitric oxide synthase 3 Rattus norvegicus 67-71 23979266-8 2014 Fluvastatin enhanced myocardial endothelial nitric oxide synthase (eNOS) protein levels and increased eNOS, vascular endothelial growth factor, and hypoxia-inducible factor-1alpha mRNA expression. Fluvastatin 0-11 nitric oxide synthase 3 Rattus norvegicus 102-106 24522493-9 2014 Immunostaining showed that secretin increased intracellular stores of AQP2 and the addition of fluvastatin promoted AQP2 trafficking to the plasma membrane. Fluvastatin 95-106 aquaporin 2 Mus musculus 116-120 24521776-2 2014 Pharmacotherapy with mTOR inhibitors aggravates dyslipidemia, thus necessitating lipid-lowering therapy with fluvastatin, pravastatin, or atorvastatin. Fluvastatin 109-120 mechanistic target of rapamycin kinase Homo sapiens 21-25 23933625-8 2014 Twenty-four patients completed the study; fluvastatin significantly and reversibly reduced the levels of 6/12 (50%) biomarkers (IL1beta, VEGF, TNFalpha, IP10, sCD40L and sTF). Fluvastatin 42-53 interleukin 1 beta Homo sapiens 128-135 25151907-0 2014 [Effects of fluvastatin on expression of p38 mitogen-activated protein kinase in renal tissue of chronic graft versus host disease lupus nephritis in mice]. Fluvastatin 12-23 mitogen-activated protein kinase 14 Mus musculus 41-77 25151907-1 2014 OBJECTIVE: To explore the effects of fluvastatin on expression of p38 mitogen-activated protein kinase (p38MAPK) in renal tissue of chronic graft versus host disease (cGVHD) lupus nephritis in mice. Fluvastatin 37-48 mitogen-activated protein kinase 14 Mus musculus 66-102 25151907-1 2014 OBJECTIVE: To explore the effects of fluvastatin on expression of p38 mitogen-activated protein kinase (p38MAPK) in renal tissue of chronic graft versus host disease (cGVHD) lupus nephritis in mice. Fluvastatin 37-48 mitogen-activated protein kinase 14 Mus musculus 104-111 25151907-8 2014 CONCLUSION: The renal protection effect of fluvastatin may be achieved by inhibiting the signal pathway of p38MAPK. Fluvastatin 43-54 mitogen-activated protein kinase 14 Mus musculus 107-114 23933625-8 2014 Twenty-four patients completed the study; fluvastatin significantly and reversibly reduced the levels of 6/12 (50%) biomarkers (IL1beta, VEGF, TNFalpha, IP10, sCD40L and sTF). Fluvastatin 42-53 vascular endothelial growth factor A Homo sapiens 137-141 23933625-8 2014 Twenty-four patients completed the study; fluvastatin significantly and reversibly reduced the levels of 6/12 (50%) biomarkers (IL1beta, VEGF, TNFalpha, IP10, sCD40L and sTF). Fluvastatin 42-53 tumor necrosis factor Homo sapiens 143-151 23933625-8 2014 Twenty-four patients completed the study; fluvastatin significantly and reversibly reduced the levels of 6/12 (50%) biomarkers (IL1beta, VEGF, TNFalpha, IP10, sCD40L and sTF). Fluvastatin 42-53 C-X-C motif chemokine ligand 10 Homo sapiens 153-157 24801208-0 2014 Matrix conditions and KLF2-dependent induction of heme oxygenase-1 modulate inhibition of HCV replication by fluvastatin. Fluvastatin 109-120 Kruppel like factor 2 Homo sapiens 22-26 24846270-8 2014 Inhibition of MAPK1 and 3 phosphorylation following treatment with fluvastatin, simvastatin, and lovastatin was confirmed by western blot. Fluvastatin 67-78 mitogen-activated protein kinase 1 Mus musculus 14-19 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Fluvastatin 68-79 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 60-66 24974574-4 2014 Simvastatin, atorvastatin and lovastatin are metabolized by CYP3A4, fluvastatin by CYP2C9, while rosuvastatin by CYP2C9 and 2C19. Fluvastatin 68-79 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 83-89 24801208-0 2014 Matrix conditions and KLF2-dependent induction of heme oxygenase-1 modulate inhibition of HCV replication by fluvastatin. Fluvastatin 109-120 heme oxygenase 1 Homo sapiens 50-66 24431079-5 2014 The most effective flavonoid was orally co-administered in vivo with a cholesterol-reducing drug, fluvastatin, which is normally metabolized by CYP2C. Fluvastatin 98-109 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 144-149 24657892-0 2014 Involvement of peptidyl-prolyl isomerase Pin1 in the inhibitory effect of fluvastatin on endothelin-1-induced cardiomyocyte hypertrophy. Fluvastatin 74-85 endothelin 1 Rattus norvegicus 89-101 24657892-7 2014 KEY FINDINGS: Fluvastatin inhibited ET-1-induced increase in the cell surface area, ANP expression, and [(3)H]-leucine incorporation; and it suppressed the signaling cascade from JNK to c-Jun. Fluvastatin 14-25 mitogen-activated protein kinase 8 Rattus norvegicus 179-182 24657892-8 2014 The phosphorylated Pin1 level, an inactive form, was decreased by ET-1; however, it reached basal level by fluvastatin. Fluvastatin 107-118 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Rattus norvegicus 19-23 24657892-9 2014 Furthermore, Pin1 overexpression clearly elicited cardiomyocyte hypertrophy, which was inhibited by fluvastatin. Fluvastatin 100-111 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Rattus norvegicus 13-17 24657892-10 2014 SIGNIFICANCE: This is the first report that ET-1-induced cardiomyocyte hypertrophy is mediated through the Pin1 activation and that the inhibitory effect of fluvastatin on cardiomyocyte hypertrophy would partly be attributed to the suppression of the Pin1 function. Fluvastatin 157-168 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Rattus norvegicus 251-255 24657892-0 2014 Involvement of peptidyl-prolyl isomerase Pin1 in the inhibitory effect of fluvastatin on endothelin-1-induced cardiomyocyte hypertrophy. Fluvastatin 74-85 peptidylprolyl cis/trans isomerase, NIMA-interacting 1 Rattus norvegicus 41-45 24905317-6 2014 Finally, the influence of fluvastatin on cell migration and production of MMP-9 and VEGF was determined using a wound-healing assay and ELISA test, respectively. Fluvastatin 26-37 matrix metallopeptidase 9 Rattus norvegicus 74-79 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Fluvastatin 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 25614710-0 2014 Fluvastatin upregulates the alpha 1C subunit of CaV1.2 channel expression in vascular smooth muscle cells via RhoA and ERK/p38 MAPK pathways. Fluvastatin 0-11 ras homolog family member A Homo sapiens 110-114 25614710-0 2014 Fluvastatin upregulates the alpha 1C subunit of CaV1.2 channel expression in vascular smooth muscle cells via RhoA and ERK/p38 MAPK pathways. Fluvastatin 0-11 mitogen-activated protein kinase 1 Homo sapiens 119-122 25614710-0 2014 Fluvastatin upregulates the alpha 1C subunit of CaV1.2 channel expression in vascular smooth muscle cells via RhoA and ERK/p38 MAPK pathways. Fluvastatin 0-11 mitogen-activated protein kinase 1 Homo sapiens 123-126 25614710-0 2014 Fluvastatin upregulates the alpha 1C subunit of CaV1.2 channel expression in vascular smooth muscle cells via RhoA and ERK/p38 MAPK pathways. Fluvastatin 0-11 mitogen-activated protein kinase 3 Homo sapiens 127-131 25614710-10 2014 Inhibition of ROCK, ERK, or p38 MAPK activation largely enhanced the upregulation effect of fluvastatin (P < 0.01). Fluvastatin 92-103 mitogen-activated protein kinase 1 Homo sapiens 20-23 25614710-10 2014 Inhibition of ROCK, ERK, or p38 MAPK activation largely enhanced the upregulation effect of fluvastatin (P < 0.01). Fluvastatin 92-103 mitogen-activated protein kinase 1 Homo sapiens 28-31 25614710-10 2014 Inhibition of ROCK, ERK, or p38 MAPK activation largely enhanced the upregulation effect of fluvastatin (P < 0.01). Fluvastatin 92-103 mitogen-activated protein kinase 3 Homo sapiens 32-36 25614710-13 2014 Fluvastatin upregulated LTCCalpha 1C expression, at least in part, by inhibiting ROCK, ERK1/2, and p38 MAPK activation. Fluvastatin 0-11 mitogen-activated protein kinase 3 Homo sapiens 87-93 25614710-13 2014 Fluvastatin upregulated LTCCalpha 1C expression, at least in part, by inhibiting ROCK, ERK1/2, and p38 MAPK activation. Fluvastatin 0-11 mitogen-activated protein kinase 1 Homo sapiens 99-102 25614710-13 2014 Fluvastatin upregulated LTCCalpha 1C expression, at least in part, by inhibiting ROCK, ERK1/2, and p38 MAPK activation. Fluvastatin 0-11 mitogen-activated protein kinase 3 Homo sapiens 103-107 24905317-6 2014 Finally, the influence of fluvastatin on cell migration and production of MMP-9 and VEGF was determined using a wound-healing assay and ELISA test, respectively. Fluvastatin 26-37 vascular endothelial growth factor A Rattus norvegicus 84-88 24905317-9 2014 CONCLUSION: The inhibitory effects of fluvastatin on cell proliferation seemed to be associated with decreased p-ERK1/2 expression, upregulation of p-JNK1/2, and reduction in the MMP-9 and VEGF concentrations in culture media. Fluvastatin 38-49 mitogen activated protein kinase 3 Rattus norvegicus 113-119 24905317-9 2014 CONCLUSION: The inhibitory effects of fluvastatin on cell proliferation seemed to be associated with decreased p-ERK1/2 expression, upregulation of p-JNK1/2, and reduction in the MMP-9 and VEGF concentrations in culture media. Fluvastatin 38-49 matrix metallopeptidase 9 Rattus norvegicus 179-184 24905317-9 2014 CONCLUSION: The inhibitory effects of fluvastatin on cell proliferation seemed to be associated with decreased p-ERK1/2 expression, upregulation of p-JNK1/2, and reduction in the MMP-9 and VEGF concentrations in culture media. Fluvastatin 38-49 vascular endothelial growth factor A Rattus norvegicus 189-193 24337703-6 2014 Fluvastatin sensitivity was associated with an estrogen receptor alpha (ERalpha)-negative, basal-like tumor subtype, features that can be scored with routine and/or strong preclinical diagnostics. Fluvastatin 0-11 estrogen receptor 1 Homo sapiens 47-70 24337703-6 2014 Fluvastatin sensitivity was associated with an estrogen receptor alpha (ERalpha)-negative, basal-like tumor subtype, features that can be scored with routine and/or strong preclinical diagnostics. Fluvastatin 0-11 estrogen receptor 1 Homo sapiens 72-79 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Fluvastatin 118-129 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 207-213 24484539-5 2014 Among the substrates that are preferably metabolized by CYP3A4, including carebastine, itraconazole, haloperidol, and fluvastatin, the former three compounds were found to closely dock to the heme region of CYP3A4 but not to that of CYP3A5. Fluvastatin 118-129 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 233-239 23996477-0 2013 Quantitative assessment of the contribution of sodium-dependent taurocholate co-transporting polypeptide (NTCP) to the hepatic uptake of rosuvastatin, pitavastatin and fluvastatin. Fluvastatin 168-179 solute carrier family 10 member 1 Homo sapiens 106-110 24604047-4 2014 RESULTS: Fluvastatin induced apoptosis in a dose- and time-dependent manner in TNFalpha -stimulated SW982 human synovial cells. Fluvastatin 9-20 tumor necrosis factor Homo sapiens 79-87 24209962-0 2013 Autophagy contributes to apoptosis in A20 and EL4 lymphoma cells treated with fluvastatin. Fluvastatin 78-89 tumor necrosis factor, alpha-induced protein 3 Mus musculus 38-41 24209962-0 2013 Autophagy contributes to apoptosis in A20 and EL4 lymphoma cells treated with fluvastatin. Fluvastatin 78-89 epilepsy 4 Mus musculus 46-49 24209962-4 2013 We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells. Fluvastatin 14-25 caspase 3 Mus musculus 93-102 24209962-4 2013 We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells. Fluvastatin 14-25 BCL2-associated X protein Mus musculus 107-110 24209962-4 2013 We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells. Fluvastatin 14-25 B cell leukemia/lymphoma 2 Mus musculus 169-174 24209962-4 2013 We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells. Fluvastatin 14-25 tumor necrosis factor, alpha-induced protein 3 Mus musculus 203-206 24209962-4 2013 We found that fluvastatin treatment enhanced the activation of pro-apoptotic members such as caspase-3 and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells. Fluvastatin 14-25 epilepsy 4 Mus musculus 211-214 24209962-8 2013 Fluvastatin-induced activation of caspase-3, DNA fragmentation, and activation of LC3-II were blocked by metabolic products of the HMG-CoA reductase reaction, such as mevalonate, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP). Fluvastatin 0-11 caspase 3 Mus musculus 34-43 24604047-5 2014 A geranylgeranylpyrophosphate (GGPP) inhibitor, but not a farnesylpyrophosphate (FPP) inhibitor, induced apoptosis, and fluvastatin-induced apoptosis was associated with the translocation of isoprenylated RhoA and Rac1 proteins from the cell membrane to the cytosol. Fluvastatin 120-131 ras homolog family member A Homo sapiens 205-209 24604047-5 2014 A geranylgeranylpyrophosphate (GGPP) inhibitor, but not a farnesylpyrophosphate (FPP) inhibitor, induced apoptosis, and fluvastatin-induced apoptosis was associated with the translocation of isoprenylated RhoA and Rac1 proteins from the cell membrane to the cytosol. Fluvastatin 120-131 Rac family small GTPase 1 Homo sapiens 214-218 24604047-6 2014 Fluvastatin-induced downstream apoptotic signals were associated with inhibition of the phosphoinositide 3-kinase (PI3K)/Akt pathway. Fluvastatin 0-11 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta Homo sapiens 88-113 24604047-6 2014 Fluvastatin-induced downstream apoptotic signals were associated with inhibition of the phosphoinositide 3-kinase (PI3K)/Akt pathway. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 121-124 24604047-8 2014 INTERPRETATION & CONCLUSIONS: Collectively, our data indicate that fluvastatin induces apoptotic cell death in TNFalpha-stimulated SW982 human synovial cells through the inactivation of the geranylgerenylated membrane fraction of RhoA and Rac1 proteins and the subsequent inhibition of the PI3K/Akt signaling pathway. Fluvastatin 71-82 tumor necrosis factor Homo sapiens 115-123 24604047-8 2014 INTERPRETATION & CONCLUSIONS: Collectively, our data indicate that fluvastatin induces apoptotic cell death in TNFalpha-stimulated SW982 human synovial cells through the inactivation of the geranylgerenylated membrane fraction of RhoA and Rac1 proteins and the subsequent inhibition of the PI3K/Akt signaling pathway. Fluvastatin 71-82 ras homolog family member A Homo sapiens 234-238 24604047-8 2014 INTERPRETATION & CONCLUSIONS: Collectively, our data indicate that fluvastatin induces apoptotic cell death in TNFalpha-stimulated SW982 human synovial cells through the inactivation of the geranylgerenylated membrane fraction of RhoA and Rac1 proteins and the subsequent inhibition of the PI3K/Akt signaling pathway. Fluvastatin 71-82 Rac family small GTPase 1 Homo sapiens 243-247 24604047-8 2014 INTERPRETATION & CONCLUSIONS: Collectively, our data indicate that fluvastatin induces apoptotic cell death in TNFalpha-stimulated SW982 human synovial cells through the inactivation of the geranylgerenylated membrane fraction of RhoA and Rac1 proteins and the subsequent inhibition of the PI3K/Akt signaling pathway. Fluvastatin 71-82 AKT serine/threonine kinase 1 Homo sapiens 299-302 23996477-3 2013 The present study revisited the interaction of statin drugs, including pitavastatin, fluvastatin and rosuvastatin, with the sodium-dependent taurocholate co-transporting polypeptide (NTCP) using gene transfected cell models. Fluvastatin 85-96 solute carrier family 10 member 1 Homo sapiens 183-187 24254555-9 2013 Simvastatin and fluvastatin but not cerivastatin, were able to inhibit the HGF-depending migration and showed a significant effect on the inhibition of the isoprenylation (GGPP). Fluvastatin 16-27 hepatocyte growth factor Homo sapiens 75-78 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 285-296 pleiotrophin Homo sapiens 141-153 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 285-296 pleiotrophin Homo sapiens 155-158 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 285-296 vascular endothelial growth factor A Homo sapiens 200-204 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 298-301 pleiotrophin Homo sapiens 141-153 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 298-301 pleiotrophin Homo sapiens 155-158 24042838-1 2013 The aim of the present study was to investigate the effect of a high-glucose-based peritoneal dialysis solution (HGPDS) on the expression of pleiotrophin (PTN) and vascular endothelial growth factor (VEGF) in human peritoneal mesothelial cells (HPMCs) and the mechanisms through which fluvastatin (Flu) protects the peritoneal membrane in continuous ambulatory peritoneal dialysis (CAPD). Fluvastatin 298-301 vascular endothelial growth factor A Homo sapiens 200-204 24042838-14 2013 GSK650394 and PD98059 significantly decreased the high mRNA and protein expression levels of PTN and VEGF induced by HGPDS (P<0.05) and Flu had the same inhibitory effect as GSK650394 and PD98059 in a dose-dependent manner (P<0.05). Fluvastatin 139-142 pleiotrophin Homo sapiens 93-96 24042838-14 2013 GSK650394 and PD98059 significantly decreased the high mRNA and protein expression levels of PTN and VEGF induced by HGPDS (P<0.05) and Flu had the same inhibitory effect as GSK650394 and PD98059 in a dose-dependent manner (P<0.05). Fluvastatin 139-142 vascular endothelial growth factor A Homo sapiens 101-105 24042838-17 2013 The results from the present study indicated that HGPDS increased the expression of PTN and VEGF in the HPMCs, and this increase was attenuated by Flu, GSK650394 and PD98059. Fluvastatin 147-150 pleiotrophin Homo sapiens 84-87 24042838-17 2013 The results from the present study indicated that HGPDS increased the expression of PTN and VEGF in the HPMCs, and this increase was attenuated by Flu, GSK650394 and PD98059. Fluvastatin 147-150 vascular endothelial growth factor A Homo sapiens 92-96 24042838-19 2013 Taken together, the protective effects of Flu in HPMCs may be partially achieved through the SGK1-ERK1/2 signaling pathway. Fluvastatin 42-45 serum/glucocorticoid regulated kinase 1 Homo sapiens 93-97 24042838-19 2013 Taken together, the protective effects of Flu in HPMCs may be partially achieved through the SGK1-ERK1/2 signaling pathway. Fluvastatin 42-45 mitogen-activated protein kinase 3 Homo sapiens 98-104 24417081-0 2013 [Inhibitory effects of fluvastatin on activation of THP-1 cells induced by anti-beta2GPI/beta2GPI complex]. Fluvastatin 23-34 GLI family zinc finger 2 Homo sapiens 52-57 24417081-1 2013 This study is to explore the interventional effects of fluvastatin on anti-beta2GPI/beta2GPI-induced activation in THP-1 mononuclear cells. Fluvastatin 55-66 apolipoprotein H Homo sapiens 75-83 24417081-0 2013 [Inhibitory effects of fluvastatin on activation of THP-1 cells induced by anti-beta2GPI/beta2GPI complex]. Fluvastatin 23-34 apolipoprotein H Homo sapiens 80-88 24417081-1 2013 This study is to explore the interventional effects of fluvastatin on anti-beta2GPI/beta2GPI-induced activation in THP-1 mononuclear cells. Fluvastatin 55-66 apolipoprotein H Homo sapiens 84-92 24417081-1 2013 This study is to explore the interventional effects of fluvastatin on anti-beta2GPI/beta2GPI-induced activation in THP-1 mononuclear cells. Fluvastatin 55-66 GLI family zinc finger 2 Homo sapiens 115-120 24417081-0 2013 [Inhibitory effects of fluvastatin on activation of THP-1 cells induced by anti-beta2GPI/beta2GPI complex]. Fluvastatin 23-34 apolipoprotein H Homo sapiens 89-97 24417081-2 2013 In vitro, human mononuclear cells THP-1 were treated with fluvastatin, LPS and anti-beta2GPI/beta2GPI, then the TF expression on THP-1 cells was detected by real-time quantitative PCR (RT-qPCR) or TF activity was detected by kit. Fluvastatin 58-69 GLI family zinc finger 2 Homo sapiens 34-39 24040034-4 2013 The lipophilic statins, fluvastatin and simvastatin, reversed LPS-induced downregulation of CD9 and CD81, simultaneously preventing TNF-alpha and matrix metalloproteinase-9 production and spreading of RAW264.7 cells. Fluvastatin 24-35 CD9 antigen Mus musculus 92-95 24417081-6 2013 Fluvastatin (50 mg x L(-1)) could decrease TF (mRNA and activity) expression and the level of TNF-alpha (mRNA and protein) in THP-1 cells with anti-beta2GPI/beta2GPI complex. Fluvastatin 0-11 tumor necrosis factor Homo sapiens 94-103 24417081-6 2013 Fluvastatin (50 mg x L(-1)) could decrease TF (mRNA and activity) expression and the level of TNF-alpha (mRNA and protein) in THP-1 cells with anti-beta2GPI/beta2GPI complex. Fluvastatin 0-11 GLI family zinc finger 2 Homo sapiens 126-131 24417081-6 2013 Fluvastatin (50 mg x L(-1)) could decrease TF (mRNA and activity) expression and the level of TNF-alpha (mRNA and protein) in THP-1 cells with anti-beta2GPI/beta2GPI complex. Fluvastatin 0-11 apolipoprotein H Homo sapiens 148-156 24417081-6 2013 Fluvastatin (50 mg x L(-1)) could decrease TF (mRNA and activity) expression and the level of TNF-alpha (mRNA and protein) in THP-1 cells with anti-beta2GPI/beta2GPI complex. Fluvastatin 0-11 apolipoprotein H Homo sapiens 157-165 24417081-9 2013 And these effects of anti-beta2GPI/beta2GPI complex could be blocked by fluvastatin. Fluvastatin 72-83 apolipoprotein H Homo sapiens 26-34 24417081-9 2013 And these effects of anti-beta2GPI/beta2GPI complex could be blocked by fluvastatin. Fluvastatin 72-83 apolipoprotein H Homo sapiens 35-43 24417081-10 2013 In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha. Fluvastatin 15-26 nuclear factor kappa B subunit 1 Homo sapiens 74-83 24417081-10 2013 In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha. Fluvastatin 15-26 apolipoprotein H Homo sapiens 149-157 24417081-10 2013 In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha. Fluvastatin 15-26 apolipoprotein H Homo sapiens 158-166 24417081-10 2013 In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha. Fluvastatin 15-26 GLI family zinc finger 2 Homo sapiens 184-189 24417081-10 2013 In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha. Fluvastatin 15-26 tumor necrosis factor Homo sapiens 236-245 24040034-4 2013 The lipophilic statins, fluvastatin and simvastatin, reversed LPS-induced downregulation of CD9 and CD81, simultaneously preventing TNF-alpha and matrix metalloproteinase-9 production and spreading of RAW264.7 cells. Fluvastatin 24-35 CD81 antigen Mus musculus 100-104 24040034-4 2013 The lipophilic statins, fluvastatin and simvastatin, reversed LPS-induced downregulation of CD9 and CD81, simultaneously preventing TNF-alpha and matrix metalloproteinase-9 production and spreading of RAW264.7 cells. Fluvastatin 24-35 tumor necrosis factor Mus musculus 132-141 24040034-4 2013 The lipophilic statins, fluvastatin and simvastatin, reversed LPS-induced downregulation of CD9 and CD81, simultaneously preventing TNF-alpha and matrix metalloproteinase-9 production and spreading of RAW264.7 cells. Fluvastatin 24-35 matrix metallopeptidase 9 Mus musculus 146-172 23846727-1 2013 Our recent in vitro experiments suggest that fluvastatin may influence tyrosinase (key enzyme of melanogenesis) synthesis. Fluvastatin 45-56 tyrosinase Mus musculus 71-81 24024895-0 2013 CYP2C9 and ABCG2 polymorphisms as risk factors for developing adverse drug reactions in renal transplant patients taking fluvastatin: a case-control study. Fluvastatin 121-132 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 24024895-0 2013 CYP2C9 and ABCG2 polymorphisms as risk factors for developing adverse drug reactions in renal transplant patients taking fluvastatin: a case-control study. Fluvastatin 121-132 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 11-16 24024895-1 2013 AIM: To investigate whether an association exists between fluvastatin-induced adverse drug reactions (ADRs) and polymorphisms in genes encoding the metabolizing enzyme CYP2C9 and the drug transporter ABCG2 in renal transplant recipients (RTRs). Fluvastatin 58-69 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 168-174 24024895-1 2013 AIM: To investigate whether an association exists between fluvastatin-induced adverse drug reactions (ADRs) and polymorphisms in genes encoding the metabolizing enzyme CYP2C9 and the drug transporter ABCG2 in renal transplant recipients (RTRs). Fluvastatin 58-69 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 200-205 24024895-8 2013 CONCLUSION: Our preliminary data demonstrate an association between fluvastatin-induced ADRs in RTRs and genetic variants in the CYP2C9 and ABCG2 genes. Fluvastatin 68-79 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 129-135 24024895-8 2013 CONCLUSION: Our preliminary data demonstrate an association between fluvastatin-induced ADRs in RTRs and genetic variants in the CYP2C9 and ABCG2 genes. Fluvastatin 68-79 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 140-145 23846727-5 2013 The expression of tyrosinase was reduced in the presence of fluvastatin. Fluvastatin 60-71 tyrosinase Mus musculus 18-28 23212095-9 2013 After fluvastatin treatment, immunohistochemical analysis of tumor cells showed a decrease in vascular endothelial growth factor receptor-2 expression by 86% and an increase in caspase-3 by 8.5%. Fluvastatin 6-17 kinase insert domain receptor Rattus norvegicus 94-139 23198837-0 2013 Fluvastatin inhibits the induction of inducible nitric oxide synthase, an inflammatory biomarker, in hepatocytes. Fluvastatin 0-11 nitric oxide synthase 2 Rattus norvegicus 38-69 23198837-11 2013 Fluvastatin decreased the levels of iNOS protein and its mRNA expression. Fluvastatin 0-11 nitric oxide synthase 2 Rattus norvegicus 36-40 23198837-14 2013 Transfection experiments demonstrated that fluvastatin suppressed iNOS induction by the inhibition of promoter transactivation and mRNA stabilization. Fluvastatin 43-54 nitric oxide synthase 2 Rattus norvegicus 66-70 23198837-15 2013 Fluvastatin reduced the expression of an iNOS gene antisense-transcript, which is involved in iNOS mRNA stability. Fluvastatin 0-11 nitric oxide synthase 2 Rattus norvegicus 41-45 23198837-15 2013 Fluvastatin reduced the expression of an iNOS gene antisense-transcript, which is involved in iNOS mRNA stability. Fluvastatin 0-11 nitric oxide synthase 2 Rattus norvegicus 94-98 23198837-16 2013 CONCLUSION: Results indicate that fluvastatin inhibits the induction of iNOS at both transcriptional and post-transcriptional steps, leading to the prevention of NO production. Fluvastatin 34-45 nitric oxide synthase 2 Rattus norvegicus 72-76 23198837-17 2013 Fluvastatin may provide therapeutic potential in iNOS induction involved in various liver injuries. Fluvastatin 0-11 nitric oxide synthase 2 Rattus norvegicus 49-53 23212095-9 2013 After fluvastatin treatment, immunohistochemical analysis of tumor cells showed a decrease in vascular endothelial growth factor receptor-2 expression by 86% and an increase in caspase-3 by 8.5%. Fluvastatin 6-17 caspase 3 Rattus norvegicus 177-186 23776402-0 2013 Effects of Fluvastatin on the Pharmacokinetics of Repaglinide: Possible Role of CYP3A4 and P-glycoprotein Inhibition by Fluvastatin. Fluvastatin 120-131 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 91-105 23959724-7 2013 Fatty acid synthase (FAS) activity was increased by the administration of fluvastatin and lovastatin, as was glucose-6-P dehydrogenase (G6PDH) by the administration of atorvastatin and lovastatin. Fluvastatin 74-85 fatty acid synthase Rattus norvegicus 0-19 23959724-7 2013 Fatty acid synthase (FAS) activity was increased by the administration of fluvastatin and lovastatin, as was glucose-6-P dehydrogenase (G6PDH) by the administration of atorvastatin and lovastatin. Fluvastatin 74-85 fatty acid synthase Rattus norvegicus 21-24 23776402-2 2013 The effect of fluvastatin on P-glycoprotein and CYP3A4 activity was evaluated. Fluvastatin 14-25 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 29-43 23776402-4 2013 Fluvastatin inhibited CYP3A4 activity in a concentration-dependent manner with a 50% inhibition concentration(IC50) of 4.1 microM and P-gp activity. Fluvastatin 0-11 phosphoglycolate phosphatase Rattus norvegicus 134-138 23776402-13 2013 Fluvastatin enhanced the oral BA of repaglinide, which may be mainly attributable to the inhibition of the CYP3A4-mediated metabolism of repaglinide in the small intestine and/or liver, to the inhibition of the P-gp efflux transporter in the small intestine and/or to the reduction of TBC of repaglinide by fluvastatin. Fluvastatin 0-11 phosphoglycolate phosphatase Rattus norvegicus 211-215 24252689-5 2013 Glioblastoma cell lines were sensitive to both drugs and a combination of 100 muM celecoxib and 240 muM fluvastatin was the most synergistic. Fluvastatin 104-115 latexin Homo sapiens 100-103 23667543-2 2013 Fluvastatin inhibited the activation of the small guanosin triphosphate binding protein (GTP) RhoA and the consequent actin redistribution induced by ligation of LFA1 involved in NK-tumor target cell adhesion. Fluvastatin 0-11 ras homolog family member A Homo sapiens 94-98 23667543-2 2013 Fluvastatin inhibited the activation of the small guanosin triphosphate binding protein (GTP) RhoA and the consequent actin redistribution induced by ligation of LFA1 involved in NK-tumor target cell adhesion. Fluvastatin 0-11 integrin subunit alpha L Homo sapiens 162-166 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 natural cytotoxicity triggering receptor 1 Homo sapiens 90-95 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 Fc gamma receptor IIIa Homo sapiens 104-108 23667543-3 2013 Also, fluvastatin reduced ganglioside M1 rafts formation triggered through the engagement of NK cell activating receptors as FcgammaRIIIA (CD16), NKG2D and DNAM1. Fluvastatin 6-17 Fc gamma receptor IIIa Homo sapiens 125-137 23667543-10 2013 Likewise, antibody dependent cellular cytotoxicity (ADCC) triggered through FcgammaRIIIA engagement with the humanized monoclonal antibody rituximab or trastuzumab was only marginally affected in fluvastatin-treated NK cells. Fluvastatin 196-207 Fc gamma receptor IIIa Homo sapiens 76-88 23667543-3 2013 Also, fluvastatin reduced ganglioside M1 rafts formation triggered through the engagement of NK cell activating receptors as FcgammaRIIIA (CD16), NKG2D and DNAM1. Fluvastatin 6-17 Fc gamma receptor IIIa Homo sapiens 139-143 23667543-3 2013 Also, fluvastatin reduced ganglioside M1 rafts formation triggered through the engagement of NK cell activating receptors as FcgammaRIIIA (CD16), NKG2D and DNAM1. Fluvastatin 6-17 killer cell lectin like receptor K1 Homo sapiens 146-151 23667543-3 2013 Also, fluvastatin reduced ganglioside M1 rafts formation triggered through the engagement of NK cell activating receptors as FcgammaRIIIA (CD16), NKG2D and DNAM1. Fluvastatin 6-17 CD226 molecule Homo sapiens 156-161 23667543-4 2013 Cytolysis of tumor targets was inhibited up to 90% when NK cells were cultured with fluvastatin by affecting i) receptor-mediated increase of the intracellular free calcium concentration, ii) activation of akt1/PKB and iii) perforin and granzyme release. Fluvastatin 84-95 AKT serine/threonine kinase 1 Homo sapiens 206-222 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 killer cell lectin like receptor K1 Homo sapiens 54-59 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 CD226 molecule Homo sapiens 61-71 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 natural cytotoxicity triggering receptor 3 Homo sapiens 73-78 23667543-5 2013 Fluvastatin displayed a stronger inhibiting effect on NKG2D, DNAM1, 2B4, NKp30, NKp44 and NKp46 than on CD16-mediated NK cell triggering. Fluvastatin 0-11 natural cytotoxicity triggering receptor 2 Homo sapiens 80-85 23717538-3 2013 Simvastatin and fluvastatin induced HO-1. Fluvastatin 16-27 heme oxygenase 1 Mus musculus 36-40 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 320-331 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 23717538-6 2013 In RAW 264.7 cells, both statins increased the activity of reporter genes linked to the proximal 1.3 kbp promoter of HO-1 (EC50 of 1.4+-0.3 microM for simvastatin and 0.6+-0.03 microM for fluvastatin). Fluvastatin 188-199 heme oxygenase 1 Mus musculus 117-121 22641573-16 2013 CONCLUSION: These results suggest that fluvastatin reduces high glucose-induced NF-kappaB activation via the p38MAPK pathway in renal tubular epithelial cells in vivo and in vitro. Fluvastatin 39-50 mitogen activated protein kinase 14 Rattus norvegicus 109-116 23449454-4 2013 Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival. Fluvastatin 23-34 caspase 3 Mus musculus 144-153 23449454-4 2013 Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival. Fluvastatin 23-34 poly (ADP-ribose) polymerase family, member 1 Mus musculus 155-159 23449454-4 2013 Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival. Fluvastatin 23-34 BCL2-associated X protein Mus musculus 164-167 23449454-4 2013 Statins (atorvastatin, fluvastatin and simvastatin) treatment enhanced the DNA fragmentation and the activation of proapoptotic members such as caspase-3, PARP and Bax, but suppressed the activation of anti-apoptotic molecule Bcl-2 in lymphoma cells including A20 and EL4 cells, which was accompanied by inhibition of cell survival. Fluvastatin 23-34 B cell leukemia/lymphoma 2 Mus musculus 226-231 22941809-0 2012 CYP2C9*3(1075A>C), MDR1 G2677T/A and MDR1 C3435T are determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 101-112 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 22941809-0 2012 CYP2C9*3(1075A>C), MDR1 G2677T/A and MDR1 C3435T are determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 101-112 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 22941809-0 2012 CYP2C9*3(1075A>C), MDR1 G2677T/A and MDR1 C3435T are determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 101-112 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 22941809-1 2012 To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers. Fluvastatin 127-138 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 68-74 23283573-12 2013 With experiments using NO synthase (NOS) blockade with L-NAME, NOS activation with fluvastatin or NO supplementation with SNAP, we demonstrated that beta3-ARs and VEGF are functionally coupled via the NO pathway. Fluvastatin 83-94 calcium channel, voltage-dependent, beta 3 subunit Mus musculus 149-154 23283573-12 2013 With experiments using NO synthase (NOS) blockade with L-NAME, NOS activation with fluvastatin or NO supplementation with SNAP, we demonstrated that beta3-ARs and VEGF are functionally coupled via the NO pathway. Fluvastatin 83-94 vascular endothelial growth factor A Mus musculus 163-167 22941809-1 2012 To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers. Fluvastatin 127-138 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 320-331 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 22941809-1 2012 To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers. Fluvastatin 127-138 solute carrier organic anion transporter family member 1B1 Homo sapiens 82-89 22927251-0 2012 Fluvastatin inhibits FLT3 glycosylation in human and murine cells and prolongs survival of mice with FLT3/ITD leukemia. Fluvastatin 0-11 fms related receptor tyrosine kinase 3 Homo sapiens 21-25 22941809-1 2012 To evaluate the impact of single-nucleotide polymorphisms (SNPs) in CYP2C9, MDR1, SLCO1B1 and ABCG2 on the pharmacokinetics of fluvastatin in Chinese participants.A pharmacokinetic study of fluvastatin (single dose 40 mg) was conducted in 12 healthy Chinese volunteers. Fluvastatin 127-138 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 94-99 22941809-4 2012 The SNPs were determined by TaqMan (MGB) genotyping assay.Effect of CYP2C9*3 (c.1075A>C) on area under the plasma concentration-time curve (AUC) of fluvastatin was statistically significant. Fluvastatin 151-162 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 68-74 22941809-7 2012 MDR1 C3435T polymorphism had a significant effect on maximal plasma concentrations (C max) of fluvastatin. Fluvastatin 94-105 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 189-200 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 189-200 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 189-200 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 22941809-10 2012 Some SNPs such as MDR1 C1236T, ABCG2 c.34G>A, ABCG2 c.421C>A, SLCO1B1 c.388 A>G, SLCO1B1 c.521 T>C, SLCO1B1 c.571 T>C and SLCO1B1 c.597 C>T have no significant effects on fluvastatin pharmacokinetics.CYP2C9*3(1075A>C), MDR1 C3435T and MDR1 G2677T/A were determinants of inter-subject variability in fluvastatin pharmacokinetics in healthy Chinese volunteers. Fluvastatin 320-331 solute carrier organic anion transporter family member 1B1 Homo sapiens 90-97 22689023-4 2012 Simvastatin or fluvastatin induced a significant increase in HO-1 protein expression and mRNA levels. Fluvastatin 15-26 heme oxygenase 1 Mus musculus 61-65 22689023-7 2012 Gel retardation experiments for C/EBP and upstream stimulatory factor (USF) DNA-binding activities using simvastatin- or fluvastatin-treated cells showed significant nuclear protein-DNA complexes which were supershifted with antibodies specific for C/EBP beta and delta or USF-1 and USF-2. Fluvastatin 121-132 CCAAT/enhancer binding protein (C/EBP), alpha Mus musculus 32-37 22689023-7 2012 Gel retardation experiments for C/EBP and upstream stimulatory factor (USF) DNA-binding activities using simvastatin- or fluvastatin-treated cells showed significant nuclear protein-DNA complexes which were supershifted with antibodies specific for C/EBP beta and delta or USF-1 and USF-2. Fluvastatin 121-132 CCAAT/enhancer binding protein (C/EBP), beta Mus musculus 249-259 22689023-7 2012 Gel retardation experiments for C/EBP and upstream stimulatory factor (USF) DNA-binding activities using simvastatin- or fluvastatin-treated cells showed significant nuclear protein-DNA complexes which were supershifted with antibodies specific for C/EBP beta and delta or USF-1 and USF-2. Fluvastatin 121-132 upstream transcription factor 1 Mus musculus 273-278 22689023-7 2012 Gel retardation experiments for C/EBP and upstream stimulatory factor (USF) DNA-binding activities using simvastatin- or fluvastatin-treated cells showed significant nuclear protein-DNA complexes which were supershifted with antibodies specific for C/EBP beta and delta or USF-1 and USF-2. Fluvastatin 121-132 upstream transcription factor 2 Mus musculus 283-288 22927251-5 2012 Growth inhibition studies indicate that FLT3/ITD-expressing cells were killed with an IC(50) within a range of 0.2-2muM fluvastatin. Fluvastatin 120-131 FMS-like tyrosine kinase 3 Mus musculus 40-44 22927251-7 2012 An increase in the IC(50) for inhibition of phosphorylated FLT3/ITD by lestaurtinib caused by exogenous FLT3 ligand, resistance to sorafenib caused by the D835Y or FLT3/ITD N676K mutations, and activation of the IL-3 compensatory pathway were all negated by fluvastatin treatment. Fluvastatin 258-269 FMS-like tyrosine kinase 3 Mus musculus 59-63 22927251-8 2012 Finally, fluvastatin treatment in vivo reduced engraftment of BaF3 FLT3/ITD cells in Balb/c mice. Fluvastatin 9-20 FMS-like tyrosine kinase 3 Mus musculus 67-71 22148003-9 2011 In conclusion, fluvastatin should be used with caution in patients with liver cirrhosis, especially with other medications metabolized with CYP2C9. Fluvastatin 15-26 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 140-146 22356114-5 2012 Our study shows that atorvastatin and fluvastatin induce proteolytic activation of PKCdelta in the APL NB4 cell line, which expresses the t(15;17) translocation. Fluvastatin 38-49 protein kinase C delta Homo sapiens 83-91 22847201-0 2012 Lipid-lowering effect of fluvastatin in relation to cytochrome P450 2C9 variant alleles frequently distributed in the Czech population. Fluvastatin 25-36 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 52-71 22847201-1 2012 BACKGROUND: CYP2C9*3 allele has been reported to correlate with increased plasma concentration of fluvastatin active form in healthy volunteers. Fluvastatin 98-109 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 12-18 22847201-2 2012 We analyzed the correlation between the CYP2C9 genotype and cholesterol-lowering effect of fluvastatin in human hypercholesterolemic patients. Fluvastatin 91-102 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 40-46 22847201-4 2012 CYP2C9 genotype was determined by PCR-RFLP assay in 87 patients on concomitant fluvastatin therapy, in 48 patients on monotherapy, and in a control group of 254 healthy volunteers of Czech nationality. Fluvastatin 79-90 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 22847201-10 2012 CONCLUSIONS: In hypercholesterolemic patients, LDL-C serum concentration was decreased more significantly in fluvastatin-treated subjects bearing the CYP2C9*1/*3 genotype compared to CYP2C9*1/*1 genotype. Fluvastatin 109-120 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 150-156 22847201-10 2012 CONCLUSIONS: In hypercholesterolemic patients, LDL-C serum concentration was decreased more significantly in fluvastatin-treated subjects bearing the CYP2C9*1/*3 genotype compared to CYP2C9*1/*1 genotype. Fluvastatin 109-120 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 183-189 21947850-0 2012 Fluvastatin inhibits angiotensin II-induced nuclear factor kappa B activation in renal tubular epithelial cells through the p38 MAPK pathway. Fluvastatin 0-11 angiotensinogen Rattus norvegicus 21-35 21947850-0 2012 Fluvastatin inhibits angiotensin II-induced nuclear factor kappa B activation in renal tubular epithelial cells through the p38 MAPK pathway. Fluvastatin 0-11 mitogen activated protein kinase 14 Rattus norvegicus 124-127 21947850-2 2012 Here, we investigate the effect of fluvastatin on activation of nuclear factor-kappaB (NF-kappaB) induced by angiotensin II (AngII) in rat kidney tubule epithelial cells (NRK-52E). Fluvastatin 35-46 angiotensinogen Rattus norvegicus 109-123 21947850-2 2012 Here, we investigate the effect of fluvastatin on activation of nuclear factor-kappaB (NF-kappaB) induced by angiotensin II (AngII) in rat kidney tubule epithelial cells (NRK-52E). Fluvastatin 35-46 angiotensinogen Rattus norvegicus 125-130 21947850-9 2012 Incubation of cells with fluvastatin significantly inhibited the AngII-induced NF-kappaB activation in a dose-dependent (10(-7)-10(-5) mol/l) manner (P < 0.05). Fluvastatin 25-36 angiotensinogen Rattus norvegicus 65-70 21947850-11 2012 These results suggest the fluvastatin reduced AngII-induced NF-kappaB activation via the p38MAPK pathway in NRK-52E cells. Fluvastatin 26-37 angiotensinogen Rattus norvegicus 46-51 21947850-11 2012 These results suggest the fluvastatin reduced AngII-induced NF-kappaB activation via the p38MAPK pathway in NRK-52E cells. Fluvastatin 26-37 mitogen activated protein kinase 14 Rattus norvegicus 89-96 22811596-7 2012 For fluvastatin IR capsule 40 mg BID, C(max) was 283 +- 271 and 382 +- 255 ng/mL, and AUC(0-24 h) was 720 +- 776 and 917 +- 994 ng h/mL on day 1 and day 7, respectively. Fluvastatin 4-15 BH3 interacting domain death agonist Homo sapiens 33-36 22811596-8 2012 The relative bioavailability of fluvastatin ER tablet 80 mg QD to fluvastatin IR capsule 40 mg BID is (45.3 +- 23.9)% and (43.3 +- 24.1)% on day 1 and day 7, respectively. Fluvastatin 32-43 BH3 interacting domain death agonist Homo sapiens 95-98 22301944-6 2012 METHODS: We investigated the effect of fluvastatin on Abeta metabolism at a clinically relevant dose in mice. Fluvastatin 39-50 amyloid beta (A4) precursor protein Mus musculus 54-59 22113336-4 2011 The data revealed that, in the atherosclerotic animal model, the protein HMGB1 and its gene expression were increased and that fluvastatin treatment significantly reduced the release of HMGB1 into the extracellular space. Fluvastatin 127-138 high mobility group box 1 Homo sapiens 186-191 22863265-10 2012 Being male and major genotype IL28B single nucleotide polymorphisms (SNPs) were independent predictive factors for SVR among patients on fluvastatin with multivariate analysis. Fluvastatin 137-148 interferon lambda 3 Homo sapiens 30-35 22863265-12 2012 Male and major genotype IL28B SNPs were independent predictors for SVR among patients on fluvastatin combination therapy. Fluvastatin 89-100 interferon lambda 3 Homo sapiens 24-29 22396501-4 2012 Therefore, we investigated the effect of fluvastatin on hypoxia-induced human ET-1 expression in vascular smooth muscle cells (VSMC). Fluvastatin 41-52 endothelin 1 Homo sapiens 78-82 22396501-7 2012 Under concentrations of 1 micromol/L or greater, fluvastatin attenuated the hypoxia-induced ET-1 gene expression through the accelerated ubiquitin/proteasome-dependent degradation of HIF-1alpha, thus consequently attenuating HIF-1alpha binding to the HRE of the ET-1 gene. Fluvastatin 49-60 endothelin 1 Homo sapiens 92-96 22396501-7 2012 Under concentrations of 1 micromol/L or greater, fluvastatin attenuated the hypoxia-induced ET-1 gene expression through the accelerated ubiquitin/proteasome-dependent degradation of HIF-1alpha, thus consequently attenuating HIF-1alpha binding to the HRE of the ET-1 gene. Fluvastatin 49-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 183-193 22396501-7 2012 Under concentrations of 1 micromol/L or greater, fluvastatin attenuated the hypoxia-induced ET-1 gene expression through the accelerated ubiquitin/proteasome-dependent degradation of HIF-1alpha, thus consequently attenuating HIF-1alpha binding to the HRE of the ET-1 gene. Fluvastatin 49-60 hypoxia inducible factor 1 subunit alpha Homo sapiens 225-235 22396501-7 2012 Under concentrations of 1 micromol/L or greater, fluvastatin attenuated the hypoxia-induced ET-1 gene expression through the accelerated ubiquitin/proteasome-dependent degradation of HIF-1alpha, thus consequently attenuating HIF-1alpha binding to the HRE of the ET-1 gene. Fluvastatin 49-60 endothelin 1 Homo sapiens 262-266 22396501-9 2012 CONCLUSION: The present study suggests that fluvastatin attenuates HIF-1-dependent ET-1 gene expression in conjunction with the stimulation of HIF-1alpha ubiquitin/proteasome-dependent degradation via isoprenoid-dependent mechanisms. Fluvastatin 44-55 hypoxia inducible factor 1 subunit alpha Homo sapiens 67-72 22396501-9 2012 CONCLUSION: The present study suggests that fluvastatin attenuates HIF-1-dependent ET-1 gene expression in conjunction with the stimulation of HIF-1alpha ubiquitin/proteasome-dependent degradation via isoprenoid-dependent mechanisms. Fluvastatin 44-55 endothelin 1 Homo sapiens 83-87 22396501-9 2012 CONCLUSION: The present study suggests that fluvastatin attenuates HIF-1-dependent ET-1 gene expression in conjunction with the stimulation of HIF-1alpha ubiquitin/proteasome-dependent degradation via isoprenoid-dependent mechanisms. Fluvastatin 44-55 hypoxia inducible factor 1 subunit alpha Homo sapiens 143-153 22594566-10 2012 During inhibition with fluvastatin, a lack of equivalence was observed with AUC(INF)(LS-GMR [90%CI] = 1.25 [1.16-1.34]) and AUC(96) (1.2 [1.13=1.27]). Fluvastatin 23-34 colony stimulating factor 2 receptor subunit alpha Homo sapiens 88-91 22222818-3 2012 Here, we investigate the action of fluvastatin and other cholesterol depleting agents on native and recombinant human P2X(4) receptor. Fluvastatin 35-46 purinergic receptor P2X 4 Homo sapiens 118-124 22222818-4 2012 Fluvastatin and mbetaCD suppressed P2X(4)-dependent calcium influx in THP-1 monocytes, without affecting P2Y receptor responses. Fluvastatin 0-11 purinergic receptor P2X 4 Homo sapiens 35-41 22222818-4 2012 Fluvastatin and mbetaCD suppressed P2X(4)-dependent calcium influx in THP-1 monocytes, without affecting P2Y receptor responses. Fluvastatin 0-11 GLI family zinc finger 2 Homo sapiens 70-75 22222818-8 2012 These data suggest fluvastatin suppresses P2X(4) activity in monocytes through cholesterol depletion and not by modulating intrinsic channel properties. Fluvastatin 19-30 purinergic receptor P2X 4 Homo sapiens 42-48 21093076-0 2012 Fluvastatin upregulates endothelial nitric oxide synthase activity via enhancement of its phosphorylation and expression and via an increase in tetrahydrobiopterin in vascular endothelial cells. Fluvastatin 0-11 nitric oxide synthase 3 Homo sapiens 24-57 21093076-3 2012 RESULTS: Fluvastatin was observed to enhance eNOS phosphorylation at Ser-1177 and Ser-633 through the PI3-kinase/Akt and PKA pathways, respectively. Fluvastatin 9-20 AKT serine/threonine kinase 1 Homo sapiens 113-116 21093076-5 2012 The mRNA of GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme of the first step of de novo BH4 synthesis, as well as eNOS, was upregulated in HUVEC treated with fluvastatin. Fluvastatin 166-177 GTP cyclohydrolase 1 Homo sapiens 12-32 21093076-5 2012 The mRNA of GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme of the first step of de novo BH4 synthesis, as well as eNOS, was upregulated in HUVEC treated with fluvastatin. Fluvastatin 166-177 GTP cyclohydrolase 1 Homo sapiens 34-39 21093076-10 2012 In addition to modulating eNOS, fluvastatin potentiates GTPCH gene expression and BH4 synthesis, thereby increasing NO production and preventing relative shortages of BH4. Fluvastatin 32-43 GTP cyclohydrolase 1 Homo sapiens 56-61 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Fluvastatin 96-107 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 119-125 21820929-6 2012 RESULTS: CYP3A4 was responsible for the metabolism of lovastatin, simvastatin and atorvastatin; fluvastatin depends on CYP2C9; P-glycoprotein is responsible for decreased atorvastatin, pravastatin, simvastatin and lovastatin concentrations. Fluvastatin 96-107 ATP binding cassette subfamily B member 1 Homo sapiens 127-141 21858457-0 2011 Fluvastatin modulates renal water reabsorption in vivo through increased AQP2 availability at the apical plasma membrane of collecting duct cells. Fluvastatin 0-11 aquaporin 2 Mus musculus 73-77 21945488-0 2011 Interaction of fluvastatin with the liver-specific Na+ -dependent taurocholate cotransporting polypeptide (NTCP). Fluvastatin 15-26 solute carrier family 10 member 1 Homo sapiens 107-111 21945488-3 2011 Here, we studied whether Na(+)-dependent taurocholate co-transporting polypeptide (NTCP, SLC10A1) can be an alternative hepatic uptake route for fluvastatin. Fluvastatin 145-156 solute carrier family 10 member 1 Homo sapiens 83-87 21945488-3 2011 Here, we studied whether Na(+)-dependent taurocholate co-transporting polypeptide (NTCP, SLC10A1) can be an alternative hepatic uptake route for fluvastatin. Fluvastatin 145-156 solute carrier family 10 member 1 Homo sapiens 89-96 21945488-6 2011 Fluvastatin appeared to be a potent and competitive inhibitor of [(3)H]-TCA uptake (IC(50) of 40muM), pointing to an interaction at the level of the bile acid binding pocket of NTCP. Fluvastatin 0-11 solute carrier family 10 member 1 Homo sapiens 177-181 21945488-8 2011 Studies in CHO-NTCP cells showed that fluvastatin was indeed an NTCP substrate (K(m) 250+-30muM, V(max) 1340+-50ng/mg total cell protein/min). Fluvastatin 38-49 solute carrier family 10 member 1 Homo sapiens 15-19 21945488-8 2011 Studies in CHO-NTCP cells showed that fluvastatin was indeed an NTCP substrate (K(m) 250+-30muM, V(max) 1340+-50ng/mg total cell protein/min). Fluvastatin 38-49 solute carrier family 10 member 1 Homo sapiens 64-68 21945488-10 2011 In conclusion, fluvastatin interacts with NTCP at the level of the bile acid binding pocket and is an NTCP substrate. Fluvastatin 15-26 solute carrier family 10 member 1 Homo sapiens 42-46 21945488-10 2011 In conclusion, fluvastatin interacts with NTCP at the level of the bile acid binding pocket and is an NTCP substrate. Fluvastatin 15-26 solute carrier family 10 member 1 Homo sapiens 102-106 21394808-1 2011 Currently used hypolipidemic drugs, Fluvastatin and Atorvastatin, act via inhibiting the rate-limiting enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase of the mevalonate pathway. Fluvastatin 36-47 3-hydroxy-3-methylglutaryl-coenzyme A reductase Mesocricetus auratus 110-168 21213109-5 2011 We show that the promoter activity of prostacyclin synthase (PTGIS), the mRNA expression of PTGIS and endothelial nitric oxide synthase (eNOS), and the production of PGI2 and NO are significantly induced by fluvastatin. Fluvastatin 207-218 prostaglandin I2 synthase Homo sapiens 38-59 21213109-5 2011 We show that the promoter activity of prostacyclin synthase (PTGIS), the mRNA expression of PTGIS and endothelial nitric oxide synthase (eNOS), and the production of PGI2 and NO are significantly induced by fluvastatin. Fluvastatin 207-218 prostaglandin I2 synthase Homo sapiens 61-66 21213109-5 2011 We show that the promoter activity of prostacyclin synthase (PTGIS), the mRNA expression of PTGIS and endothelial nitric oxide synthase (eNOS), and the production of PGI2 and NO are significantly induced by fluvastatin. Fluvastatin 207-218 prostaglandin I2 synthase Homo sapiens 92-97 21213109-5 2011 We show that the promoter activity of prostacyclin synthase (PTGIS), the mRNA expression of PTGIS and endothelial nitric oxide synthase (eNOS), and the production of PGI2 and NO are significantly induced by fluvastatin. Fluvastatin 207-218 nitric oxide synthase 3 Homo sapiens 102-135 21858457-6 2011 Consistent with this observation, fluvastatin is able to increase AQP2 membrane expression in the collecting duct of treated mice. Fluvastatin 34-45 aquaporin 2 Mus musculus 66-70 21858457-7 2011 Additional in vivo and in vitro experiments indicate that these effects of fluvastatin are most likely caused by fluvastatin-dependent changes in the prenylation status of key proteins regulating AQP2 trafficking in collecting duct cells. Fluvastatin 75-86 aquaporin 2 Mus musculus 196-200 21858457-7 2011 Additional in vivo and in vitro experiments indicate that these effects of fluvastatin are most likely caused by fluvastatin-dependent changes in the prenylation status of key proteins regulating AQP2 trafficking in collecting duct cells. Fluvastatin 113-124 aquaporin 2 Mus musculus 196-200 21824198-7 2011 In the chemotaxis migration assay, pretreatment with fluvastatin and simvastatin inhibited the migration of human CD4+ T cells towards CCL20. Fluvastatin 53-64 C-C motif chemokine ligand 20 Homo sapiens 135-140 21965734-0 2011 Fluvastatin enhances sorafenib cytotoxicity in melanoma cells via modulation of AKT and JNK signaling pathways. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 80-83 21965734-8 2011 Fluvastatin enhances sorafenib-mediated apoptosis as revealed through enhanced cleavage of poly (ADP-ribose) polymerase. Fluvastatin 0-11 poly(ADP-ribose) polymerase 1 Homo sapiens 91-119 21710988-4 2011 The results indicate that OATP2B1-mediated transport is significant for rosuvastatin, fluvastatin and atorvastatin, at neutral pH. Fluvastatin 86-97 solute carrier organic anion transporter family member 2B1 Homo sapiens 26-33 21862649-0 2011 Fluvastatin downregulates VEGF-A expression in TNF-alpha-induced retinal vessel tortuosity. Fluvastatin 0-11 vascular endothelial growth factor A Mus musculus 26-32 21862649-0 2011 Fluvastatin downregulates VEGF-A expression in TNF-alpha-induced retinal vessel tortuosity. Fluvastatin 0-11 tumor necrosis factor Mus musculus 47-56 21862649-1 2011 PURPOSE: To investigate the effect of tumor necrosis factor alpha (TNF-alpha) on the mouse retinal vasculature, function, and expression of vascular endothelial growth factor-A (VEGF-A) in the retina and retinal pigment epithelium (RPE) and to evaluate the protective effect of statin therapy (fluvastatin) on retinal vascular and functional changes. Fluvastatin 294-305 vascular endothelial growth factor A Mus musculus 178-184 21620829-3 2011 The pharmacological evaluations proved that the relaxation responses induced by fluvastatin and pravastatin were significantly inhibited by nitric oxide synthase inhibitor, N(G)-nitro-l-arginine, and cyclooxygenase inhibitor, indomethacin, while these responses were significantly increased by angiotensin converting enzyme inhibitors, captopril and enalapril, and rho kinase inhibitor, Y27632. Fluvastatin 80-91 angiotensin I converting enzyme Homo sapiens 294-323 21620829-6 2011 The experimental results indicate that activation of nitric oxide synthase and phospholipase A(2)-cyclooxygenase pathway and inhibition of angiotensin converting enzyme and rho kinase may have a role on the effects of fluvastatin and pravastatin in the human saphenous vein grafts. Fluvastatin 218-229 angiotensin I converting enzyme Homo sapiens 139-168 20827284-0 2011 Effects of fluvastatin on insulin resistance and cardiac morphology in hypertensive patients. Fluvastatin 11-22 insulin Homo sapiens 26-33 20827284-8 2011 In hypertensive patients, fluvastatin can improve maximum systolic EBP, myocardial remodelling and insulin resistance, independently of lipid profile variations and endothelial function. Fluvastatin 26-37 insulin Homo sapiens 99-106 21862649-9 2011 VEGF-A expression was significantly upregulated in the retina and RPE of TNF-alpha-injected mice, and this was significantly downregulated in fluvastatin-treated mice. Fluvastatin 142-153 vascular endothelial growth factor A Mus musculus 0-6 21862649-9 2011 VEGF-A expression was significantly upregulated in the retina and RPE of TNF-alpha-injected mice, and this was significantly downregulated in fluvastatin-treated mice. Fluvastatin 142-153 tumor necrosis factor Mus musculus 73-82 21862649-10 2011 CONCLUSIONS: This study shows that the TNF-alpha-induced inflammatory process results in the alteration of retinal microvasculature and function, and fluvastatin could be a potential therapy for treating/preventing retinal microvascular or inflammatory complications. Fluvastatin 150-161 tumor necrosis factor Mus musculus 39-48 21710988-13 2011 The present results indicate that OATP2B1 may be involved in the tissue uptake of rosuvastatin and fluvastatin, while OATP2B1 may play a significant role in the intestinal absorption of several statins due to their transporter affinity at acidic pH. Fluvastatin 99-110 solute carrier organic anion transporter family member 2B1 Homo sapiens 34-41 21447733-8 2011 Results indicate that atorvastatin, fluvastatin, and rosuvastatin were transported by P-gp, BCRP, and MRP2. Fluvastatin 36-47 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 21047568-3 2011 The objective of this study was to determine whether fluvastatin prevents the APR to zoledronic acid in post-menopausal women. Fluvastatin 53-64 phorbol-12-myristate-13-acetate-induced protein 1 Homo sapiens 78-81 21447733-8 2011 Results indicate that atorvastatin, fluvastatin, and rosuvastatin were transported by P-gp, BCRP, and MRP2. Fluvastatin 36-47 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 92-96 21447733-8 2011 Results indicate that atorvastatin, fluvastatin, and rosuvastatin were transported by P-gp, BCRP, and MRP2. Fluvastatin 36-47 ATP binding cassette subfamily C member 2 Homo sapiens 102-106 21565414-0 2011 Fluvastatin reduces the high mobility group box 1 protein expression in hyperlipidemia. Fluvastatin 0-11 high mobility group box 1 Homo sapiens 24-49 21173016-9 2011 Proteomic analysis showed proteins involved in thrombotic development (annexin II, RhoA and protein disulphide isomerase) with altered expression after fluvastatin administration. Fluvastatin 152-163 annexin A2 Homo sapiens 71-81 20127518-0 2011 The cardioprotective effect of fluvastatin on ischemic injury via down-regulation of toll-like receptor 4. Fluvastatin 31-42 toll-like receptor 4 Rattus norvegicus 85-105 20127518-5 2011 The results demonstrated that fluvastatin treatment markedly decreased ischemic injury caused by ischemia/reperfusion, and inhibited the expression levels of TLR4, TNF-alpha and NF-kappaB, all of which up-regulated by ischemia/reperfusion. Fluvastatin 30-41 toll-like receptor 4 Rattus norvegicus 158-162 20127518-5 2011 The results demonstrated that fluvastatin treatment markedly decreased ischemic injury caused by ischemia/reperfusion, and inhibited the expression levels of TLR4, TNF-alpha and NF-kappaB, all of which up-regulated by ischemia/reperfusion. Fluvastatin 30-41 tumor necrosis factor Rattus norvegicus 164-173 21467191-3 2011 We have reported previously that fluvastatin induced vacuolation and cell death in rat skeletal myofibers by depleting geranylgeranylpyrophosphate (GGPP) and suppressing small GTPases, particularly Rab (FASEB J 21:4087-4094, 2007). Fluvastatin 33-44 RAB1A, member RAS oncogene family Rattus norvegicus 198-201 21467191-6 2011 Western blot analysis revealed that Rab1A protein resided predominantly in membrane but not in cytosol in control myofibers, whereas it was opposite in fluvastatin-treated myofibers, indicating that fluvastatin inhibited Rab1A translocation from cytosol to membrane. Fluvastatin 199-210 RAB1A, member RAS oncogene family Rattus norvegicus 36-41 21467191-6 2011 Western blot analysis revealed that Rab1A protein resided predominantly in membrane but not in cytosol in control myofibers, whereas it was opposite in fluvastatin-treated myofibers, indicating that fluvastatin inhibited Rab1A translocation from cytosol to membrane. Fluvastatin 199-210 RAB1A, member RAS oncogene family Rattus norvegicus 221-226 21467191-7 2011 GGPP supplementation prevented the effect of fluvastatin on Rab1A translocation. Fluvastatin 45-56 RAB1A, member RAS oncogene family Rattus norvegicus 60-65 21467191-10 2011 Immunofluorescence study revealed that the distribution of an ER marker, calnexin, was restricted to the region around nucleus with fluvastatin, suggesting the inhibition of ER membrane traffic by fluvastatin. Fluvastatin 132-143 calnexin Rattus norvegicus 73-81 21467191-10 2011 Immunofluorescence study revealed that the distribution of an ER marker, calnexin, was restricted to the region around nucleus with fluvastatin, suggesting the inhibition of ER membrane traffic by fluvastatin. Fluvastatin 197-208 calnexin Rattus norvegicus 73-81 21173016-9 2011 Proteomic analysis showed proteins involved in thrombotic development (annexin II, RhoA and protein disulphide isomerase) with altered expression after fluvastatin administration. Fluvastatin 152-163 ras homolog family member A Homo sapiens 83-87 21173016-10 2011 In-vitro studies indicated that the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase by fluvastatin might inhibit protein prenylation and MAPK activation. Fluvastatin 101-112 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 50-97 20158569-9 2011 Simvastatin, atorvastatin, fluvastatin or pravastatin reduced the IL-6 production by 53%, 50%, 64% and 60%, respectively. Fluvastatin 27-38 interleukin 6 Homo sapiens 66-70 21309808-13 2011 The inhibitory function of fluvastatin on key components of intraperitoneal inflammatory angiogenesis shown in the present study is clearly associated with the modulatory effects of this statin on vascular endothelial growth factor, TNF-alpha and NO production. Fluvastatin 27-38 tumor necrosis factor Mus musculus 233-242 20696189-4 2011 Atorvastatin (10, 20 mg/kg), simvastatin (30 mg/kg) and fluvastatin (10 mg/kg) treatment significantly attenuated the quinolinic acid induced behavioral (locomotor activity, rotarod performance and beam walk test), biochemical (lipid peroxidation, nitrite concentration, SOD and catalase), mitochondrial enzyme complex alterations in rats suggesting their free radical scavenging potential. Fluvastatin 56-67 catalase Rattus norvegicus 279-287 21091218-12 2011 Additionally, fluvastatin suppressed CD40 expression in all three genotypes. Fluvastatin 14-25 CD40 molecule Homo sapiens 37-41 21460414-11 2011 Analogously, mRNA expression of conjugative enzyme Ugt1a1 was diminished by fluvastatin administration to cholestatic rats. Fluvastatin 76-87 UDP glucuronosyltransferase family 1 member A1 Rattus norvegicus 51-57 21174002-4 2011 Fluvastatin treatment increased t-PA expression more than 10-fold and reduced PAI-1 expression up to five-fold. Fluvastatin 0-11 plasminogen activator, tissue type Homo sapiens 32-36 21174002-4 2011 Fluvastatin treatment increased t-PA expression more than 10-fold and reduced PAI-1 expression up to five-fold. Fluvastatin 0-11 serpin family E member 1 Homo sapiens 78-83 21174002-9 2011 Inhibition of p38, as well as p38alpha or p38beta siRNA, reversed the effects of fluvastatin on t-PA expression. Fluvastatin 81-92 mitogen-activated protein kinase 14 Homo sapiens 14-17 21174002-9 2011 Inhibition of p38, as well as p38alpha or p38beta siRNA, reversed the effects of fluvastatin on t-PA expression. Fluvastatin 81-92 mitogen-activated protein kinase 14 Homo sapiens 30-38 21174002-9 2011 Inhibition of p38, as well as p38alpha or p38beta siRNA, reversed the effects of fluvastatin on t-PA expression. Fluvastatin 81-92 mitogen-activated protein kinase 11 Homo sapiens 42-49 21174002-9 2011 Inhibition of p38, as well as p38alpha or p38beta siRNA, reversed the effects of fluvastatin on t-PA expression. Fluvastatin 81-92 plasminogen activator, tissue type Homo sapiens 96-100 21174002-10 2011 Treatment with p38beta siRNA partially reversed the effect of fluvastatin on PAI-1, whereas p38alpha siRNA had no significant effect. Fluvastatin 62-73 mitogen-activated protein kinase 11 Homo sapiens 15-22 21174002-10 2011 Treatment with p38beta siRNA partially reversed the effect of fluvastatin on PAI-1, whereas p38alpha siRNA had no significant effect. Fluvastatin 62-73 serpin family E member 1 Homo sapiens 77-82 21174002-11 2011 Inhibition of jun kinase reduced basal and fluvastatin-induced t-PA expression to the same extent and increased PAI-1. Fluvastatin 43-54 plasminogen activator, tissue type Homo sapiens 63-67 21174002-11 2011 Inhibition of jun kinase reduced basal and fluvastatin-induced t-PA expression to the same extent and increased PAI-1. Fluvastatin 43-54 serpin family E member 1 Homo sapiens 112-117 21174002-13 2011 In human EC, the fluvastatin-induced increase in t-PA is mediated by Cdc42 and, as with t-PA induced by inhibition of actin polymerisation, requires activation of p38MAP kinase. Fluvastatin 17-28 plasminogen activator, tissue type Homo sapiens 49-53 21174002-13 2011 In human EC, the fluvastatin-induced increase in t-PA is mediated by Cdc42 and, as with t-PA induced by inhibition of actin polymerisation, requires activation of p38MAP kinase. Fluvastatin 17-28 cell division cycle 42 Homo sapiens 69-74 21174002-13 2011 In human EC, the fluvastatin-induced increase in t-PA is mediated by Cdc42 and, as with t-PA induced by inhibition of actin polymerisation, requires activation of p38MAP kinase. Fluvastatin 17-28 plasminogen activator, tissue type Homo sapiens 88-92 21174002-14 2011 The mechanisms by which fluvastatin treatment reduces PAI-1 are different from those that increase t-PA. Fluvastatin 24-35 serpin family E member 1 Homo sapiens 54-59 24212635-8 2011 Both fluvastatin and zoledronic acid inhibited Ras and Rap prenylation, and the phosphorylation of ERK1/2 and AKT. Fluvastatin 5-16 LDL receptor related protein associated protein 1 Homo sapiens 55-58 24212635-10 2011 CONCLUSIONS: Zoledronic acid enhances fluvastatin and paclitaxel activity against T24 in a synergistic manner and this is mediated largely by inhibition of both the Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways via isoprenylation inhibition. Fluvastatin 38-49 zinc fingers and homeoboxes 2 Homo sapiens 169-172 24212635-10 2011 CONCLUSIONS: Zoledronic acid enhances fluvastatin and paclitaxel activity against T24 in a synergistic manner and this is mediated largely by inhibition of both the Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways via isoprenylation inhibition. Fluvastatin 38-49 mitogen-activated protein kinase kinase 7 Homo sapiens 173-176 24212635-10 2011 CONCLUSIONS: Zoledronic acid enhances fluvastatin and paclitaxel activity against T24 in a synergistic manner and this is mediated largely by inhibition of both the Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways via isoprenylation inhibition. Fluvastatin 38-49 mitogen-activated protein kinase 1 Homo sapiens 177-180 24212635-10 2011 CONCLUSIONS: Zoledronic acid enhances fluvastatin and paclitaxel activity against T24 in a synergistic manner and this is mediated largely by inhibition of both the Ras/Raf/MEK/ERK and PI3K/AKT signaling pathways via isoprenylation inhibition. Fluvastatin 38-49 AKT serine/threonine kinase 1 Homo sapiens 190-193 20696189-5 2011 Additionally, atorvastatin (10, 20 mg/kg), simvastatin (30 mg/kg) and fluvastatin (10 mg/kg) significantly decrease the TNF-alpha level and striatal lesion volume in quinolinic acid treated animals indicating their anti-inflammatory effects. Fluvastatin 70-81 tumor necrosis factor Rattus norvegicus 120-129 21362314-0 2011 Fluvastatin attenuates myocardial interstitial fibrosis and cardiac dysfunction in diabetic rats by inhibiting over-expression of connective tissue growth factor. Fluvastatin 0-11 cellular communication network factor 2 Rattus norvegicus 130-161 21362314-11 2011 CONCLUSIONS: Fluvastatin attenuates cardiac dysfunction and myocardial interstitial fibrosis of diabetic rat by inhibiting activity of RhoA to down-regulate the overexpression of CTGF, and Rho/Rho-kinase pathway may be an important target in the treatment of diabetic cardiomyopathy. Fluvastatin 13-24 ras homolog family member A Rattus norvegicus 135-139 21362314-11 2011 CONCLUSIONS: Fluvastatin attenuates cardiac dysfunction and myocardial interstitial fibrosis of diabetic rat by inhibiting activity of RhoA to down-regulate the overexpression of CTGF, and Rho/Rho-kinase pathway may be an important target in the treatment of diabetic cardiomyopathy. Fluvastatin 13-24 cellular communication network factor 2 Rattus norvegicus 179-183 20884711-3 2011 DESIGN AND METHODS: We exposed mesenchymal stromal cells to inhibitors, such as fluvastatin, of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase, responsible for the synthesis of mevalonate, the precursor of cholesterol. Fluvastatin 80-91 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 100-147 20884711-7 2011 RESULTS: Fluvastatin altered the assembly of actin microfilaments, inactivated RhoA guanosin triphosphate binding protein, inhibited the S-phase of the cell cycle, induced apoptosis in a small fraction of cells but preserved cytokine production. Fluvastatin 9-20 ras homolog family member A Homo sapiens 79-83 21673461-11 2011 CONCLUSION: Fluvastatin reduces both UAE and the urinary L-FABP level, and thus, has renoprotective effects, independent of its lipid lowering effects in dyslipidemic patients with CKD. Fluvastatin 12-23 fatty acid binding protein 1 Homo sapiens 57-63 22041697-3 2011 Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate). Fluvastatin 221-232 solute carrier organic anion transporter family member 1B1 Homo sapiens 0-42 21826199-0 2011 Anti-inflammatory effect of fluvastatin on IL-8 production induced by Pseudomonas aeruginosa and Aspergillus fumigatus antigens in cystic fibrosis. Fluvastatin 28-39 C-X-C motif chemokine ligand 8 Homo sapiens 43-47 21826199-2 2011 Since recent research has identified the anti-inflammatory properties of statins (besides their lipid-lowering effects), we investigated the effect of fluvastatin on the production of the potent neutrophil chemoattractant chemokine, IL-8, in whole blood from CF patients, stimulated by Pseudomonas aeruginosa (LPS) and Aspergillus fumigatus (AFA) antigens. Fluvastatin 151-162 C-X-C motif chemokine ligand 8 Homo sapiens 233-237 21826199-6 2011 Fluvastatin strongly decreased the levels of IL-8, in a concentration-dependent manner, in whole blood from CF patients. Fluvastatin 0-11 C-X-C motif chemokine ligand 8 Homo sapiens 45-49 22041697-3 2011 Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate). Fluvastatin 221-232 solute carrier organic anion transporter family member 1B1 Homo sapiens 44-51 22041697-3 2011 Organic anion transporting polypeptide 1B1 (OATP1B1, gene SLCO1B1) is expressed on the basolateral membrane of hepatocytes and can facilitate hepatic uptake of certain clinically relevant drugs such as statins except for fluvastatin, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, antidiabetic drug (repaglinide) and anticancer drugs (SN-38 and methotrexate). Fluvastatin 221-232 solute carrier organic anion transporter family member 1B1 Homo sapiens 58-65 21351272-7 2010 Here we evaluate interactions between 4 statins (lovastatin, atorvastatin, fluvastatin and rosuvastatin) and P-gp, at both the molecular level using purified P-gp and at the cellular level using human MDR tumor cells. Fluvastatin 75-86 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 21351272-10 2010 Finally, fluvastatin and rosuvastatin only interacted with P-gp in vitro at high concentrations and did not inhibit doxorubicin transport in MDR cells. Fluvastatin 9-20 ATP binding cassette subfamily B member 1 Homo sapiens 59-63 20864107-0 2010 Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway. Fluvastatin 0-11 NFE2 like bZIP transcription factor 2 Homo sapiens 87-91 20851116-6 2010 Therapeutic doses of statins (pravastatin, simvastatin, atorvastatin and fluvastatin) in patients with hypercholesterolemia almost completely suppressed all of the EPO-induced effects in a concentration-dependent manner. Fluvastatin 73-84 erythropoietin Homo sapiens 164-167 20864107-4 2010 METHODS AND RESULTS: In cultured human coronary artery smooth muscle cells (hCASMCs), fluvastatin activated the nuclear translocation of Nrf2, as evaluated by Western blotting and immunocytochemical analyses. Fluvastatin 86-97 NFE2 like bZIP transcription factor 2 Homo sapiens 137-141 20864107-8 2010 Western blotting and luciferase assay revealed fluvastatin activated Nrf2 via the PI3K/Akt pathway. Fluvastatin 47-58 NFE2 like bZIP transcription factor 2 Homo sapiens 69-73 20864107-8 2010 Western blotting and luciferase assay revealed fluvastatin activated Nrf2 via the PI3K/Akt pathway. Fluvastatin 47-58 AKT serine/threonine kinase 1 Homo sapiens 87-90 20864107-11 2010 Moreover, Nrf2 siRNA markedly reduced the cytoprotective effects of fluvastatin against H(2)O(2) administration in hCASMCs. Fluvastatin 68-79 NFE2 like bZIP transcription factor 2 Homo sapiens 10-14 20864107-12 2010 CONCLUSIONS: Fluvastatin exerts cytoprotective effects against oxidative stress, inducing antioxidant genes through Nrf2/ARE in hCASMCs. Fluvastatin 13-24 NFE2 like bZIP transcription factor 2 Homo sapiens 116-120 21205474-12 2010 Western blot analysis demonstrated that the combination of celecoxib and fluvastatin significantly down-regulated p-Akt (0.23+/-0.08 versus 1.12+/-0.07 and surviving (0.50+/-0.07 versus 1.47+/-0.19) in BEL-7402 tumours compared with the control (P value is less than 0.01 for all). Fluvastatin 73-84 thymoma viral proto-oncogene 1 Mus musculus 116-119 21250597-8 2010 After fluvastatin treatment, expression of Bcl-2 and procaspase-9 were downregulated, cytochrome c (cytosolic extract), Bax and cleaved-caspase-3 protein expression were increased. Fluvastatin 6-17 BCL2 apoptosis regulator Homo sapiens 43-48 21250597-8 2010 After fluvastatin treatment, expression of Bcl-2 and procaspase-9 were downregulated, cytochrome c (cytosolic extract), Bax and cleaved-caspase-3 protein expression were increased. Fluvastatin 6-17 cytochrome c, somatic Homo sapiens 86-98 21250597-8 2010 After fluvastatin treatment, expression of Bcl-2 and procaspase-9 were downregulated, cytochrome c (cytosolic extract), Bax and cleaved-caspase-3 protein expression were increased. Fluvastatin 6-17 BCL2 associated X, apoptosis regulator Homo sapiens 120-123 21604568-0 2010 [Fluvastatin"s effect on atherogenesis in apolipoprotein-E knockout mice infected by cytomegalovirus]. Fluvastatin 1-12 apolipoprotein E Mus musculus 42-58 20671225-0 2010 Effects of add-on fluvastatin therapy in patients with chronic proteinuric nephropathy on dual renin-angiotensin system blockade: the ESPLANADE trial. Fluvastatin 18-29 renin Homo sapiens 95-100 20430391-7 2010 In in-vitro assays rosuvastatin, fluvastatin, and pitavastatin directly blocked CD4 T cell-mediated endothelial cell apoptosis and reduced T cell-expression of CD69 and TRAIL through TCR-induced Extracellar signal-Regulated Kinases (ERK) activation. Fluvastatin 33-44 CD69 molecule Homo sapiens 160-164 20430391-7 2010 In in-vitro assays rosuvastatin, fluvastatin, and pitavastatin directly blocked CD4 T cell-mediated endothelial cell apoptosis and reduced T cell-expression of CD69 and TRAIL through TCR-induced Extracellar signal-Regulated Kinases (ERK) activation. Fluvastatin 33-44 TNF superfamily member 10 Homo sapiens 169-174 20430391-7 2010 In in-vitro assays rosuvastatin, fluvastatin, and pitavastatin directly blocked CD4 T cell-mediated endothelial cell apoptosis and reduced T cell-expression of CD69 and TRAIL through TCR-induced Extracellar signal-Regulated Kinases (ERK) activation. Fluvastatin 33-44 T cell receptor beta variable 20/OR9-2 (non-functional) Homo sapiens 183-186 20809476-7 2010 Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9). Fluvastatin 0-11 cytochrome P450 2C5 Oryctolagus cuniculus 162-168 20809476-7 2010 Fluvastatin and nifedipine increased the systemic exposure of nateglinide in rabbits, probably due to their inhibitory action on the metabolism of nateglinide by CYP2C5 (human CYP2C9). Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 176-182 20671225-8 2010 Fluvastatin further reduced total and LDL cholesterol and apolipoprotein B versus benazepril-valsartan alone, but did not affect serum triglycerides and GFR. Fluvastatin 0-11 apolipoprotein B Homo sapiens 58-74 20666265-0 2010 Effects of fluvastatin therapy on serum interleukin-18 and interleukin-10 levels in patients with acute coronary syndrome. Fluvastatin 11-22 interleukin 18 Homo sapiens 40-54 20668001-1 2010 In this paper, we have investigated the mechanism of phototoxicity of fluvastatin, an 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, in human keratinocytes cell line NCTC-2544. Fluvastatin 70-81 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 86-133 21472326-8 2010 This effect was statin-specific as the down-regulation of SATB1 was brought about by hydrophobic statins, such as simvastatin and fluvastatin, but not by hydrophilic pravastatin. Fluvastatin 130-141 SATB homeobox 1 Homo sapiens 58-63 20587623-2 2010 Treatment of HF diet-fed rats with fluvastatin (8 mg/kg) was lethal, followed by an elevation in levels of plasma aspartate aminotransferase and creatine kinase activities and skeletal muscle toxicity. Fluvastatin 35-46 glutamic-oxaloacetic transaminase 2 Rattus norvegicus 114-140 20587623-7 2010 In addition, the mRNA levels of Oatp2, CYP2C11, and CYP3A1/2 were markedly decreased in HF diet-fed and fluvastatin-treated rats. Fluvastatin 104-115 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 32-37 20587623-7 2010 In addition, the mRNA levels of Oatp2, CYP2C11, and CYP3A1/2 were markedly decreased in HF diet-fed and fluvastatin-treated rats. Fluvastatin 104-115 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 39-46 20587623-7 2010 In addition, the mRNA levels of Oatp2, CYP2C11, and CYP3A1/2 were markedly decreased in HF diet-fed and fluvastatin-treated rats. Fluvastatin 104-115 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 52-58 20587623-9 2010 In liver cell nuclei, levels of constitutive androstane receptor, pregnane X receptor, and hepatocyte nuclear factor 4alpha proteins were decreased in fluvastatin-treated HF diet-fed rats, which correlated with the decrease in Oatp2, CYP2C, and CYP3A. Fluvastatin 151-162 hepatocyte nuclear factor 4, alpha Rattus norvegicus 32-123 20587623-9 2010 In liver cell nuclei, levels of constitutive androstane receptor, pregnane X receptor, and hepatocyte nuclear factor 4alpha proteins were decreased in fluvastatin-treated HF diet-fed rats, which correlated with the decrease in Oatp2, CYP2C, and CYP3A. Fluvastatin 151-162 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 227-232 20587623-9 2010 In liver cell nuclei, levels of constitutive androstane receptor, pregnane X receptor, and hepatocyte nuclear factor 4alpha proteins were decreased in fluvastatin-treated HF diet-fed rats, which correlated with the decrease in Oatp2, CYP2C, and CYP3A. Fluvastatin 151-162 cytochrome P450, subfamily 2, polypeptide 11 Rattus norvegicus 234-239 20587623-9 2010 In liver cell nuclei, levels of constitutive androstane receptor, pregnane X receptor, and hepatocyte nuclear factor 4alpha proteins were decreased in fluvastatin-treated HF diet-fed rats, which correlated with the decrease in Oatp2, CYP2C, and CYP3A. Fluvastatin 151-162 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 245-250 20472556-0 2010 Reduction of brain beta-amyloid (Abeta) by fluvastatin, a hydroxymethylglutaryl-CoA reductase inhibitor, through increase in degradation of amyloid precursor protein C-terminal fragments (APP-CTFs) and Abeta clearance. Fluvastatin 43-54 amyloid beta (A4) precursor protein Mus musculus 19-39 20472556-10 2010 In cultured brain microvessel endothelial cells, fluvastatin increased LRP1 and the uptake of Abeta, which was blocked by LRP1 antagonists, through an isoprenoid-dependent mechanism. Fluvastatin 49-60 low density lipoprotein receptor-related protein 1 Mus musculus 71-75 20472556-10 2010 In cultured brain microvessel endothelial cells, fluvastatin increased LRP1 and the uptake of Abeta, which was blocked by LRP1 antagonists, through an isoprenoid-dependent mechanism. Fluvastatin 49-60 low density lipoprotein receptor-related protein 1 Mus musculus 122-126 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 cyclin dependent kinase inhibitor 1A Homo sapiens 108-111 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 cyclin dependent kinase inhibitor 1A Homo sapiens 112-116 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 cyclin dependent kinase inhibitor 1A Homo sapiens 117-121 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 AKT serine/threonine kinase 1 Homo sapiens 146-149 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 151-175 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 MCL1 apoptosis regulator, BCL2 family member Homo sapiens 177-182 20926014-4 2010 The combination of celecoxib and fluvastatin also increased levels of the cyclin-dependent kinase inhibitor p21(Waf1/Cip1), decreased levels of p-Akt, myeloid cell leukaemia-1 (Mcl-1) and survivin protein, but had no effect on Akt protein levels in tumours. Fluvastatin 33-44 AKT serine/threonine kinase 1 Homo sapiens 227-230 20666265-0 2010 Effects of fluvastatin therapy on serum interleukin-18 and interleukin-10 levels in patients with acute coronary syndrome. Fluvastatin 11-22 interleukin 10 Homo sapiens 59-73 20666265-2 2010 Statins were shown to downregulate inflammatory cytokines.We conducted this study to investigate the effects of fluvastatin therapy on plasma interleukin-18 (IL-18) and interleukin-10 (IL-10) concentration in patients with acute coronary syndrome. Fluvastatin 112-123 interleukin 18 Homo sapiens 142-156 20666265-2 2010 Statins were shown to downregulate inflammatory cytokines.We conducted this study to investigate the effects of fluvastatin therapy on plasma interleukin-18 (IL-18) and interleukin-10 (IL-10) concentration in patients with acute coronary syndrome. Fluvastatin 112-123 interleukin 18 Homo sapiens 158-163 20666265-2 2010 Statins were shown to downregulate inflammatory cytokines.We conducted this study to investigate the effects of fluvastatin therapy on plasma interleukin-18 (IL-18) and interleukin-10 (IL-10) concentration in patients with acute coronary syndrome. Fluvastatin 112-123 interleukin 10 Homo sapiens 169-183 20666265-2 2010 Statins were shown to downregulate inflammatory cytokines.We conducted this study to investigate the effects of fluvastatin therapy on plasma interleukin-18 (IL-18) and interleukin-10 (IL-10) concentration in patients with acute coronary syndrome. Fluvastatin 112-123 interleukin 10 Homo sapiens 185-190 20360626-0 2010 Fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 melanoma cells. Fluvastatin 0-11 tyrosinase Mus musculus 22-32 20053524-8 2010 Fluvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, significantly attenuated PAAC induced left ventricular cardiac hypertrophy and MABP whereas no significant change was observed in CST-induced cardiac hypertrophy. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 13-70 20360620-3 2010 Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP. Fluvastatin 26-37 nitric oxide synthase 3 Homo sapiens 122-126 20360620-3 2010 Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP. Fluvastatin 26-37 nitric oxide synthase 3 Homo sapiens 173-177 20178046-5 2010 Fluvastatin, which is metabolized by CYP2C9, is less prone to pharmacokinetic interactions, while pravastatin, rosuvastatin and pitavastatin are not susceptible to any CYP inhibition. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 37-43 20360626-0 2010 Fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 melanoma cells. Fluvastatin 0-11 pro-opiomelanocortin-alpha Mus musculus 54-90 20360626-1 2010 The aim of this study was to evaluate the effect of fluvastatin on the alpha-melanocyte-stimulating hormone-mediated increase in tyrosinase activity in the melanoma B16F10 cell line and to establish whether Akt and extracellular signal-regulated kinase (Erk) inhibition is involved in tyrosinase synthesis after fluvastatin administration. Fluvastatin 52-63 pro-opiomelanocortin-alpha Mus musculus 71-107 20360626-1 2010 The aim of this study was to evaluate the effect of fluvastatin on the alpha-melanocyte-stimulating hormone-mediated increase in tyrosinase activity in the melanoma B16F10 cell line and to establish whether Akt and extracellular signal-regulated kinase (Erk) inhibition is involved in tyrosinase synthesis after fluvastatin administration. Fluvastatin 52-63 tyrosinase Mus musculus 129-139 20360626-1 2010 The aim of this study was to evaluate the effect of fluvastatin on the alpha-melanocyte-stimulating hormone-mediated increase in tyrosinase activity in the melanoma B16F10 cell line and to establish whether Akt and extracellular signal-regulated kinase (Erk) inhibition is involved in tyrosinase synthesis after fluvastatin administration. Fluvastatin 312-323 pro-opiomelanocortin-alpha Mus musculus 71-107 20360626-2 2010 Fluvastatin modulates alpha-melanocyte-stimulating hormone induced melanogenesis by increasing tyrosinase mRNA production, as shown by real time PCR, or tyrosinase protein synthesis, as presented by western blot technique. Fluvastatin 0-11 pro-opiomelanocortin-alpha Mus musculus 22-58 20360626-2 2010 Fluvastatin modulates alpha-melanocyte-stimulating hormone induced melanogenesis by increasing tyrosinase mRNA production, as shown by real time PCR, or tyrosinase protein synthesis, as presented by western blot technique. Fluvastatin 0-11 tyrosinase Mus musculus 95-105 20360626-2 2010 Fluvastatin modulates alpha-melanocyte-stimulating hormone induced melanogenesis by increasing tyrosinase mRNA production, as shown by real time PCR, or tyrosinase protein synthesis, as presented by western blot technique. Fluvastatin 0-11 tyrosinase Mus musculus 153-163 20360626-3 2010 The stimulatory effect of fluvastatin on melanogenesis was, in part, induced by modulation of cell proliferation (decreased melanoma cell proliferation in G2/M phase) and possibly decrease of Akt. Fluvastatin 26-37 thymoma viral proto-oncogene 1 Mus musculus 192-195 20360626-4 2010 These findings indicate that fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 cells and reveal an unknown effect of statin use: their influence on melanin production. Fluvastatin 29-40 tyrosinase Mus musculus 51-61 20360626-4 2010 These findings indicate that fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 cells and reveal an unknown effect of statin use: their influence on melanin production. Fluvastatin 29-40 pro-opiomelanocortin-alpha Mus musculus 83-119 20214592-6 2009 CYP2C8 is a major catalyst in the metabolism of paclitaxel, amodiaquine, troglitazone, amiodarone, verapamil and ibuprofen, with a secondary role in the biotransformation of cerivastatin and fluvastatin. Fluvastatin 191-202 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 0-6 19689459-0 2009 Fluvastatin and lovastatin inhibit granulocyte macrophage-colony stimulating factor-stimulated human eosinophil adhesion to inter-cellular adhesion molecule-1 under flow conditions. Fluvastatin 0-11 colony stimulating factor 2 Homo sapiens 35-83 19689459-7 2009 RESULTS: Fluvastatin and lovastatin (both 10 nm) significantly inhibited GM-CSF-stimulated eosinophil adhesion to rhICAM-1 after 2 min (34.4+/-3.0% inhibition and 37.8+/-12.6% inhibition, respectively, n=4, P<0.05) but had no significant inhibitory effect on unstimulated eosinophil adhesion. Fluvastatin 9-20 colony stimulating factor 2 Homo sapiens 73-79 19689459-9 2009 A concentration range of fluvastatin and lovastatin inhibited GM-CSF stimulated eosinophil adhesion with significant (P<0.05) inhibition observed at low concentrations of 1 nm for both drugs. Fluvastatin 25-36 colony stimulating factor 2 Homo sapiens 62-68 19689459-11 2009 CONCLUSIONS: Inhibition of eosinophil adhesion to ICAM-1 by fluvastatin and lovastatin under physiological shear stress represent novel actions by these drugs that may inform the development of anti-inflammatory therapy for allergic disease. Fluvastatin 60-71 intercellular adhesion molecule 1 Homo sapiens 50-56 19663817-1 2009 Fluvastatin has been considered to be metabolised to 5-hydroxy fluvastatin (M-2), 6-hydroxy fluvastatin (M-3) and N-desisopropyl fluvastatin (M-5) in human liver microsomes by primarily CYP2C9. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 186-192 19228263-0 2009 Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta. Fluvastatin 62-73 natriuretic peptide B Homo sapiens 34-60 20214221-7 2009 Lovastatin administration resulted in the significant decrease of the pro-inflammatory cytokines IL-6 and TNF-alfa, while that of fluvastatin brought about the significant decrease of the serum levels of IL-6, IL-8 and TNF-alfa. Fluvastatin 130-141 interleukin 6 Homo sapiens 204-208 20214221-7 2009 Lovastatin administration resulted in the significant decrease of the pro-inflammatory cytokines IL-6 and TNF-alfa, while that of fluvastatin brought about the significant decrease of the serum levels of IL-6, IL-8 and TNF-alfa. Fluvastatin 130-141 C-X-C motif chemokine ligand 8 Homo sapiens 210-214 20214221-10 2009 CONCLUSIONS: Lovastatin and fluvastatin, significantly decrease the level of viremia, of IL-6 and TNF-alpha in the patients with chronic hepatitis C. Fluvastatin 28-39 interleukin 6 Homo sapiens 89-93 20214221-10 2009 CONCLUSIONS: Lovastatin and fluvastatin, significantly decrease the level of viremia, of IL-6 and TNF-alpha in the patients with chronic hepatitis C. Fluvastatin 28-39 tumor necrosis factor Homo sapiens 98-107 19228263-0 2009 Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta. Fluvastatin 62-73 interleukin 1 alpha Homo sapiens 107-125 19228263-0 2009 Human cardiac fibroblasts express B-type natriuretic peptide: fluvastatin ameliorates its up-regulation by interleukin-1alpha, tumour necrosis factor-alpha and transforming growth factor-beta. Fluvastatin 62-73 transforming growth factor beta 1 Homo sapiens 160-191 19785645-9 2009 SLCO1B1 polymorphism also affects the pharmacokinetics of many other, but not all (fluvastatin), statins and that of the antidiabetic drug repaglinide, the antihistamine fexofenadine and the endothelin A receptor antagonist atrasentan. Fluvastatin 83-94 solute carrier organic anion transporter family member 1B1 Homo sapiens 0-7 19296953-7 2009 Fluvastatin administration decreased matrix metalloproteinase-9 expression, gelatinolytic activity, endothelial adhesion molecules expression and neutrophil infiltration, and increased type I collagen content in the cuffed region. Fluvastatin 0-11 matrix metallopeptidase 9 Mus musculus 37-63 19842935-0 2009 Different effects of the ABCG2 c.421C>A SNP on the pharmacokinetics of fluvastatin, pravastatin and simvastatin. Fluvastatin 74-85 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 25-30 19842935-7 2009 CONCLUSIONS: Genetic variability in ABCG2 markedly affects the pharmacokinetics of fluvastatin and simvastatin lactone, but has no significant effect on pravastatin or active simvastatin acid. Fluvastatin 83-94 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 36-41 19842935-1 2009 AIMS: This study aimed to investigate possible effects of the ABCG2 c.421C>A (p.Gln141Lys; rs2231142) genotype on fluvastatin, pravastatin and simvastatin pharmacokinetics. Fluvastatin 117-128 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 62-67 19726772-8 2009 Levels of total cholesterol, low-density lipoprotein cholesterol, interleukin-6, and C-reactive protein were significantly decreased in the fluvastatin group but were unchanged in the placebo group. Fluvastatin 140-151 interleukin 6 Homo sapiens 66-79 19726772-8 2009 Levels of total cholesterol, low-density lipoprotein cholesterol, interleukin-6, and C-reactive protein were significantly decreased in the fluvastatin group but were unchanged in the placebo group. Fluvastatin 140-151 C-reactive protein Homo sapiens 85-103 19467023-7 2009 Furthermore, we showed that fluvastatin or cyclosporine A in combination with IFN-alpha could prevent the relapse after therapy in the IFN-alpha-resistant HCV RNA-harboring cells. Fluvastatin 28-39 interferon alpha 1 Homo sapiens 135-144 19594754-0 2009 Fluvastatin inhibits expression of the chemokine MDC/CCL22 induced by interferon-gamma in HaCaT cells, a human keratinocyte cell line. Fluvastatin 0-11 C-C motif chemokine ligand 22 Homo sapiens 49-52 19662466-7 2009 RESULTS: MPI and AA5 uptake was best visualized in HC diet animals (n = 6) and reduced significantly after fluvastatin treatment (n = 4) or diet withdrawal (n = 3). Fluvastatin 107-118 annexin A5 Oryctolagus cuniculus 17-20 19594754-0 2009 Fluvastatin inhibits expression of the chemokine MDC/CCL22 induced by interferon-gamma in HaCaT cells, a human keratinocyte cell line. Fluvastatin 0-11 C-C motif chemokine ligand 22 Homo sapiens 53-58 19694740-1 2009 AIMS: This study aimed to investigate possible effects of ABCB1 genotype on fluvastatin, pravastatin, lovastatin, and rosuvastatin pharmacokinetics. Fluvastatin 76-87 ATP binding cassette subfamily B member 1 Homo sapiens 58-63 19594754-0 2009 Fluvastatin inhibits expression of the chemokine MDC/CCL22 induced by interferon-gamma in HaCaT cells, a human keratinocyte cell line. Fluvastatin 0-11 interferon gamma Homo sapiens 70-86 19594754-6 2009 KEY RESULTS: Fluvastatin, but not atorvastatin or simvastatin, inhibited MDC expression induced by interferon (IFN)-gamma and NF-kappaB activation. Fluvastatin 13-24 C-C motif chemokine ligand 22 Homo sapiens 73-76 19594754-6 2009 KEY RESULTS: Fluvastatin, but not atorvastatin or simvastatin, inhibited MDC expression induced by interferon (IFN)-gamma and NF-kappaB activation. Fluvastatin 13-24 interferon gamma Homo sapiens 99-121 19594754-9 2009 Interestingly, fluvastatin suppressed IFN-gamma-induced NF-kappaB activation in parallel with p38 MAPK phosphorylation. Fluvastatin 15-26 interferon gamma Homo sapiens 38-47 19594754-9 2009 Interestingly, fluvastatin suppressed IFN-gamma-induced NF-kappaB activation in parallel with p38 MAPK phosphorylation. Fluvastatin 15-26 mitogen-activated protein kinase 14 Homo sapiens 94-97 19594754-10 2009 CONCLUSIONS AND IMPLICATIONS: These results indicate that fluvastatin inhibited expression of the CC chemokine MDC induced by IFN-gamma in HaCaT cells, by inhibiting NF-kappaB activation via the p38 MAPK pathway. Fluvastatin 58-69 C-C motif chemokine ligand 22 Homo sapiens 111-114 19594754-10 2009 CONCLUSIONS AND IMPLICATIONS: These results indicate that fluvastatin inhibited expression of the CC chemokine MDC induced by IFN-gamma in HaCaT cells, by inhibiting NF-kappaB activation via the p38 MAPK pathway. Fluvastatin 58-69 interferon gamma Homo sapiens 126-135 19594754-10 2009 CONCLUSIONS AND IMPLICATIONS: These results indicate that fluvastatin inhibited expression of the CC chemokine MDC induced by IFN-gamma in HaCaT cells, by inhibiting NF-kappaB activation via the p38 MAPK pathway. Fluvastatin 58-69 mitogen-activated protein kinase 14 Homo sapiens 195-198 19442037-6 2009 All 3-hydroxyl-3-methylglutaryl-CoA reductase inhibitors (statins) except fluvastatin are substrates for OATP1B1, but hepatobiliary (canalicular) efflux transporters differ among statins. Fluvastatin 74-85 solute carrier organic anion transporter family member 1B1 Homo sapiens 105-112 19954059-0 2009 [The effect of valsartan and fluvastatin on the connective tissue growth factor expression in experimental diabetic cardiomyopathy]. Fluvastatin 29-40 cellular communication network factor 2 Rattus norvegicus 48-79 19954059-1 2009 OBJECTIVE: To investigate the effect of valsartan and fluvastatin on the expression of connective tissue growth factor in early diabetic cardiomyopathy. Fluvastatin 54-65 cellular communication network factor 2 Rattus norvegicus 87-118 19954059-8 2009 The mRNA expression of CTGF was significantly higher in the DM group than in the control group, but it was significantly lower in the valsartan group and fluvastatin group than that in the DM group (both P < 0.05). Fluvastatin 154-165 cellular communication network factor 2 Rattus norvegicus 23-27 19188342-8 2009 Phenotypic changes in podocytes, as indicated by the downregulation of nephrin, Wilms" tumour 1 and synaptopodin, along with upregulation of proliferating cell nuclear antigen, were attenuated by fluvastatin, suggesting its protective effects against podocyte injuries. Fluvastatin 196-207 nephrosis 1, nephrin Mus musculus 71-78 19188342-8 2009 Phenotypic changes in podocytes, as indicated by the downregulation of nephrin, Wilms" tumour 1 and synaptopodin, along with upregulation of proliferating cell nuclear antigen, were attenuated by fluvastatin, suggesting its protective effects against podocyte injuries. Fluvastatin 196-207 synaptopodin Mus musculus 80-112 19188342-9 2009 In cultured podocytes, angiotensin II treatment decreased nephrin expression to 13% of basal levels, which was reversed to 58% by adding fluvastatin. Fluvastatin 137-148 nephrosis 1, nephrin Mus musculus 58-65 19254730-0 2009 Fluvastatin attenuates IGF-1-induced ERK1/2 activation and cell proliferation by mevalonic acid depletion in human mesangial cells. Fluvastatin 0-11 insulin like growth factor 1 Homo sapiens 23-28 19215577-2 2009 Fluvastatin showed anti-hepatitis C virus (HCV) activity in vitro, through the inhibition of geranylgeranylation of cellular proteins, and a synergistic effect with interferon (IFN)-alpha. Fluvastatin 0-11 interferon alpha 1 Homo sapiens 165-187 19371739-13 2009 Fluvastatin increased endothelial nitric oxide synthase expression and decreased plasminogen activator inhibitor-1 expression in mature endothelial cell in the presence of sirolimus (P<0.05, respectively). Fluvastatin 0-11 serine (or cysteine) peptidase inhibitor, clade E, member 1 Mus musculus 81-114 19328808-7 2009 Moreover, cell adhesion and ROS production stimulated with MIP-1beta or AngII were completely inhibited by fluvastatin. Fluvastatin 107-118 C-C motif chemokine ligand 4 Homo sapiens 59-68 19328808-7 2009 Moreover, cell adhesion and ROS production stimulated with MIP-1beta or AngII were completely inhibited by fluvastatin. Fluvastatin 107-118 angiotensinogen Homo sapiens 72-77 19254730-0 2009 Fluvastatin attenuates IGF-1-induced ERK1/2 activation and cell proliferation by mevalonic acid depletion in human mesangial cells. Fluvastatin 0-11 mitogen-activated protein kinase 3 Homo sapiens 37-43 19254730-3 2009 We investigated the effects of fluvastatin on IGF-1-induced activation of intracellular signal pathways and MC proliferation, and examined the inhibitory mechanisms of fluvastatin. Fluvastatin 31-42 insulin like growth factor 1 Homo sapiens 46-51 19254730-6 2009 Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation. Fluvastatin 0-11 mitogen-activated protein kinase kinase 1 Homo sapiens 27-31 19254730-6 2009 Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation. Fluvastatin 0-11 insulin like growth factor 1 Homo sapiens 64-69 19254730-6 2009 Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation. Fluvastatin 0-11 mitogen-activated protein kinase kinase 1 Homo sapiens 78-84 19254730-6 2009 Fluvastatin or PD98059, an MEK1 inhibitor, completely abolished IGF-1-induced MEK1/2 and ERK1/2 phosphorylation and MC proliferation, whereas inhibition of Akt had no effect on MC proliferation. Fluvastatin 0-11 mitogen-activated protein kinase 3 Homo sapiens 89-95 19254730-7 2009 Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation. Fluvastatin 25-36 insulin like growth factor 1 Homo sapiens 51-56 19254730-7 2009 Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation. Fluvastatin 25-36 mitogen-activated protein kinase kinase 1 Homo sapiens 65-71 19254730-7 2009 Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation. Fluvastatin 25-36 mitogen-activated protein kinase 3 Homo sapiens 76-82 19254730-7 2009 Mevalonic acid prevented fluvastatin inhibition of IGF-1-induced MEK1/2 and ERK1/2 phosphorylation, cyclin D1 expression, and MC proliferation. Fluvastatin 25-36 cyclin D1 Homo sapiens 100-109 19254730-8 2009 SIGNIFICANCE: Fluvastatin inhibits IGF-1-induced activation of the MAP kinase pathway and MC proliferation by mevalonic acid depletion, and might have renoprotective effects by inhibiting IGF-1-mediated MC proliferation. Fluvastatin 14-25 insulin like growth factor 1 Homo sapiens 35-40 19254730-8 2009 SIGNIFICANCE: Fluvastatin inhibits IGF-1-induced activation of the MAP kinase pathway and MC proliferation by mevalonic acid depletion, and might have renoprotective effects by inhibiting IGF-1-mediated MC proliferation. Fluvastatin 14-25 insulin like growth factor 1 Homo sapiens 188-193 19150877-5 2009 In a small-scale human study fluvastatin activated PPARalpha and PPARgamma in platelets and reduced aggregation in response to arachidonic acid ex vivo. Fluvastatin 29-40 peroxisome proliferator activated receptor alpha Homo sapiens 51-60 19150877-5 2009 In a small-scale human study fluvastatin activated PPARalpha and PPARgamma in platelets and reduced aggregation in response to arachidonic acid ex vivo. Fluvastatin 29-40 peroxisome proliferator activated receptor gamma Homo sapiens 65-74 19220292-2 2009 Resting chloride channel conductance (gCl), carried by the ClC-1 channel, is reduced in muscles of rats chronically treated with fluvastatin, atorvastatin or fenofibrate, along with increased resting cytosolic calcium in statin-treated rats. Fluvastatin 129-140 germ cell-less 1, spermatogenesis associated Rattus norvegicus 38-41 19220292-9 2009 Accordingly, a decrease of ClC-1 channel mRNA was found in both fluvastatin- and fenofibrate-treated rat muscles. Fluvastatin 64-75 chloride voltage-gated channel 1 Rattus norvegicus 27-32 19220292-2 2009 Resting chloride channel conductance (gCl), carried by the ClC-1 channel, is reduced in muscles of rats chronically treated with fluvastatin, atorvastatin or fenofibrate, along with increased resting cytosolic calcium in statin-treated rats. Fluvastatin 129-140 chloride voltage-gated channel 1 Rattus norvegicus 59-64 19241310-10 2009 CONCLUSIONS: Pretreatment with fluvastatin seemed to reduce P-selectin levels compared to patients given placebo, and hence, we think that pretreatment with a statin, fluvastatin in our study, might reduce the perioperative cardiac injury caused by cardiopulmonary bypass-induced inflammatory changes. Fluvastatin 31-42 selectin P Homo sapiens 60-70 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 12-23 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 33-90 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 12-23 solute carrier family 8 member A1 Rattus norvegicus 112-116 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 12-23 ras homolog family member B Rattus norvegicus 159-163 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 25-28 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 33-90 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 25-28 solute carrier family 8 member A1 Rattus norvegicus 112-116 19352075-3 2009 Conversely, fluvastatin (Flv), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, decreased NCX1 mRNA and protein expression by inhibiting RhoB. Fluvastatin 25-28 ras homolog family member B Rattus norvegicus 159-163 19150166-12 2009 Pre-treatment with fluvastatin was found to improve survival rate, preserved MAP, decreased the markers of organ injury, suppressed the release of TNF-alpha and increased IL-10 after HS in rats. Fluvastatin 19-30 tumor necrosis factor Rattus norvegicus 147-156 19150166-12 2009 Pre-treatment with fluvastatin was found to improve survival rate, preserved MAP, decreased the markers of organ injury, suppressed the release of TNF-alpha and increased IL-10 after HS in rats. Fluvastatin 19-30 interleukin 10 Rattus norvegicus 171-176 19150166-13 2009 CONCLUSION: Pre-treatment with fluvastatin can suppress the release of serum TNF-alpha and can also increase serum IL-10 level to protect HS-induced multi-organ damage in rats. Fluvastatin 31-42 tumor necrosis factor Rattus norvegicus 77-86 19150166-13 2009 CONCLUSION: Pre-treatment with fluvastatin can suppress the release of serum TNF-alpha and can also increase serum IL-10 level to protect HS-induced multi-organ damage in rats. Fluvastatin 31-42 interleukin 10 Rattus norvegicus 115-120 19241310-10 2009 CONCLUSIONS: Pretreatment with fluvastatin seemed to reduce P-selectin levels compared to patients given placebo, and hence, we think that pretreatment with a statin, fluvastatin in our study, might reduce the perioperative cardiac injury caused by cardiopulmonary bypass-induced inflammatory changes. Fluvastatin 167-178 selectin P Homo sapiens 60-70 19225250-7 2009 RESULTS: Fluvastatin treatment resulted in significant decreases in levels of total cholesterol, LDL cholesterol, triglyceride (p<0.005), and C-reactive protein (p<0.05). Fluvastatin 9-20 C-reactive protein Homo sapiens 145-163 18775044-8 2009 In contrast, fluvastatin (1 microM) decreased the total nNOS in the PVs and atria. Fluvastatin 13-24 nitric oxide synthase, brain Oryctolagus cuniculus 56-60 20164019-0 2009 Fluvastatin increases tyrosinase synthesis induced by UVB irradiation of B16F10 melanoma cells. Fluvastatin 0-11 tyrosinase Mus musculus 22-32 20164019-3 2009 The role of fluvastatin, a frequently used statin, was examined in potential modulation of tyrosinase (key enzyme of melanogenesis) synthesis. Fluvastatin 12-23 tyrosinase Mus musculus 91-101 20164019-5 2009 Fluvastatin increases tyrosinase mRNA production induced by UVB irradiation in B16F10 melanoma cell line. Fluvastatin 0-11 tyrosinase Mus musculus 22-32 19129682-4 2009 L6 fibroblasts were differentiated and then treated with pravastatin, simvastatin, or fluvastatin for 72 h. Hydrophobic simvastatin and fluvastatin decreased cell viability in a dose-dependent manner via apoptosis characterized by typical nuclear fragmentation and condensation and caspase-3 activation. Fluvastatin 136-147 caspase 3 Rattus norvegicus 282-291 19129682-9 2009 Fluvastatin was continuously infused (2.08 mg/kg at an infusion rate of 0.5 mL/h) into the right internal jugular vein of the rats in vivo for 72 h. Fluvastatin infusion significantly elevated the plasma CPK level and transferred RhoA localization in the skeletal muscle from the cell membrane to the cytosol. Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 230-234 19129682-9 2009 Fluvastatin was continuously infused (2.08 mg/kg at an infusion rate of 0.5 mL/h) into the right internal jugular vein of the rats in vivo for 72 h. Fluvastatin infusion significantly elevated the plasma CPK level and transferred RhoA localization in the skeletal muscle from the cell membrane to the cytosol. Fluvastatin 149-160 ras homolog family member A Rattus norvegicus 230-234 19226708-11 2009 Fluvastatin alleviated podocyte damage and glomerular osteopontin protein expression, which was localized in podocytes. Fluvastatin 0-11 secreted phosphoprotein 1 Rattus norvegicus 54-65 19408679-0 2009 [Effects of fluvastatin on the activation of p38 mitogen-activated protein kinase in glomerular mesangial cells under high concentration of glucose]. Fluvastatin 12-23 mitogen activated protein kinase 14 Rattus norvegicus 45-81 19408679-1 2009 This study is to investigate the effects of fluvastatin on the activation of p38 mitogen-activated protein kinase (p38 MAPK) and cAMP response element-binding protein (CREB1) in glomerular mesangial cells under high concentration of glucose. Fluvastatin 44-55 mitogen activated protein kinase 14 Rattus norvegicus 77-113 19408679-1 2009 This study is to investigate the effects of fluvastatin on the activation of p38 mitogen-activated protein kinase (p38 MAPK) and cAMP response element-binding protein (CREB1) in glomerular mesangial cells under high concentration of glucose. Fluvastatin 44-55 mitogen activated protein kinase 14 Rattus norvegicus 115-123 19408679-1 2009 This study is to investigate the effects of fluvastatin on the activation of p38 mitogen-activated protein kinase (p38 MAPK) and cAMP response element-binding protein (CREB1) in glomerular mesangial cells under high concentration of glucose. Fluvastatin 44-55 cAMP responsive element binding protein 1 Rattus norvegicus 168-173 19408679-7 2009 The expression levels of p-p38 MAPK, p-CREB1, TGF-beta1 mRNA, and FN mRNA, LN and type IV collagen in the supernatants were significantly lower in the fluvastatin group than those in the high concentration glucose group. Fluvastatin 151-162 mitogen activated protein kinase 14 Rattus norvegicus 27-35 19408679-7 2009 The expression levels of p-p38 MAPK, p-CREB1, TGF-beta1 mRNA, and FN mRNA, LN and type IV collagen in the supernatants were significantly lower in the fluvastatin group than those in the high concentration glucose group. Fluvastatin 151-162 cAMP responsive element binding protein 1 Rattus norvegicus 39-44 19408679-7 2009 The expression levels of p-p38 MAPK, p-CREB1, TGF-beta1 mRNA, and FN mRNA, LN and type IV collagen in the supernatants were significantly lower in the fluvastatin group than those in the high concentration glucose group. Fluvastatin 151-162 transforming growth factor, beta 1 Rattus norvegicus 46-55 19408679-7 2009 The expression levels of p-p38 MAPK, p-CREB1, TGF-beta1 mRNA, and FN mRNA, LN and type IV collagen in the supernatants were significantly lower in the fluvastatin group than those in the high concentration glucose group. Fluvastatin 151-162 fibronectin 1 Rattus norvegicus 66-68 19408679-8 2009 It is concluded that fluvastatin can inhibit over production of TGF-beta1 and ECM proteins in GMCs under high concentration of glucose, partly by regulating the phosphorylation of p38 MAPK and CREB1. Fluvastatin 21-32 transforming growth factor, beta 1 Rattus norvegicus 64-73 19408679-8 2009 It is concluded that fluvastatin can inhibit over production of TGF-beta1 and ECM proteins in GMCs under high concentration of glucose, partly by regulating the phosphorylation of p38 MAPK and CREB1. Fluvastatin 21-32 mitogen activated protein kinase 14 Rattus norvegicus 180-188 19408679-8 2009 It is concluded that fluvastatin can inhibit over production of TGF-beta1 and ECM proteins in GMCs under high concentration of glucose, partly by regulating the phosphorylation of p38 MAPK and CREB1. Fluvastatin 21-32 cAMP responsive element binding protein 1 Rattus norvegicus 193-198 19555197-3 2009 Lovastatin and fluvastatin, two 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR) inhibitors, were used to block endogenous cholesterol biosynthesis. Fluvastatin 15-26 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 91-96 19997842-4 2009 RESULTS: During the follow-up period of 4-12 weeks, LDL-C levels were reduced by a median of 27-31% of baseline values (mean 153.1 +/- 33.5 mg/dl) mainly regardless of previous statin therapy (rosuvastatin, atorvastatin, simvastatin, pravastatin, fluvastatin, and lovastatin) and dosing (pooled median values). Fluvastatin 247-258 component of oligomeric golgi complex 2 Homo sapiens 52-57 19225250-11 2009 Following fluvastatin treatment, there were significant decreases in the mean FD of CD3 on lymphocytes, and of CD11b and CD11c on both monocytes and granulocytes (p<0.05); of these, all FD values were similar to those in the control group (p>0.05). Fluvastatin 10-21 integrin subunit alpha M Homo sapiens 111-116 19225250-11 2009 Following fluvastatin treatment, there were significant decreases in the mean FD of CD3 on lymphocytes, and of CD11b and CD11c on both monocytes and granulocytes (p<0.05); of these, all FD values were similar to those in the control group (p>0.05). Fluvastatin 10-21 integrin subunit alpha X Homo sapiens 121-126 21291779-11 2008 Further studies are also needed to determine whether concomitant administration of a non-CYP3A4-metabolized statin (such as fluvastatin, pravastatin, or rosuvastatin) with a CYP3A4 inhibitor, may reduce adverse event rates in routine clinical practice. Fluvastatin 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 89-95 21291779-11 2008 Further studies are also needed to determine whether concomitant administration of a non-CYP3A4-metabolized statin (such as fluvastatin, pravastatin, or rosuvastatin) with a CYP3A4 inhibitor, may reduce adverse event rates in routine clinical practice. Fluvastatin 124-135 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 174-180 19098381-4 2008 In the present study, we examined the effects of fluvastatin on HGF-induced angiogenesis using a human umbilical vein endothelial cell (HUVEC)/normal human dermal fibroblast (NHDF) co-culture system. Fluvastatin 49-60 hepatocyte growth factor Homo sapiens 64-67 18923248-0 2008 Short-term effects of fluvastatin therapy on plasma interleukin-10 levels in patients with chronic heart failure. Fluvastatin 22-33 interleukin 10 Homo sapiens 52-66 18923248-5 2008 We conducted this study to investigate the effects of fluvastatin therapy on plasma IL-10 cytokine concentration in patients with HF. Fluvastatin 54-65 interleukin 10 Homo sapiens 84-89 18923248-10 2008 RESULTS: A significant elevation in the plasma levels of IL-10 after 12 weeks of fluvastatin treatment (4.8+ or -1.0 vs. 6.5+ or -1.3 pg/ml, P=0.002) was observed. Fluvastatin 81-92 interleukin 10 Homo sapiens 57-62 18923248-11 2008 Plasma tumor necrosis factor-alpha levels were significantly decreased after fluvastatin therapy (6.3+ or -2.3 vs. 4.8+ or -1.4 pg/ml, P=0.003). Fluvastatin 77-88 tumor necrosis factor Homo sapiens 7-34 18923248-14 2008 CONCLUSION: Fluvastatin therapy might lead to an increase in plasma IL-10 levels and an associated improvement in vagal tonus as assessed by HRR at 1 min in patients with HF. Fluvastatin 12-23 interleukin 10 Homo sapiens 68-73 19098381-5 2008 The HGF-induced angiogenesis was augmented by fluvastatin at low dose, but it was decreased at high dose. Fluvastatin 46-57 hepatocyte growth factor Homo sapiens 4-7 19098381-6 2008 Although fluvastatin increased vascular endothelial growth factor expression in NHDFs, it was observed only at a high dose. Fluvastatin 9-20 vascular endothelial growth factor A Homo sapiens 31-65 19098381-7 2008 Low-dose fluvastatin decreased the HGF-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation (Thr-180/Tyr-182) and HUVEC apoptosis in the presence of HGF. Fluvastatin 9-20 hepatocyte growth factor Homo sapiens 35-38 19098381-7 2008 Low-dose fluvastatin decreased the HGF-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation (Thr-180/Tyr-182) and HUVEC apoptosis in the presence of HGF. Fluvastatin 9-20 mitogen-activated protein kinase 14 Homo sapiens 47-50 19098381-7 2008 Low-dose fluvastatin decreased the HGF-induced p38 mitogen-activated protein kinase (MAPK) phosphorylation (Thr-180/Tyr-182) and HUVEC apoptosis in the presence of HGF. Fluvastatin 9-20 hepatocyte growth factor Homo sapiens 164-167 19098381-9 2008 Moreover, the augmentation of the HGF-induced angiogenesis by fluvastatin was abrogated by the p38 MAPK inhibitors, SB203580, SB202190, and FR167653. Fluvastatin 62-73 hepatocyte growth factor Homo sapiens 34-37 19098381-9 2008 Moreover, the augmentation of the HGF-induced angiogenesis by fluvastatin was abrogated by the p38 MAPK inhibitors, SB203580, SB202190, and FR167653. Fluvastatin 62-73 mitogen-activated protein kinase 14 Homo sapiens 95-98 19098381-10 2008 High-dose fluvastatin decreased Akt phosphorylation (Ser-473) and HUVEC proliferation, and it increased p27(kip1) in HUVECs. Fluvastatin 10-21 interferon alpha inducible protein 27 Homo sapiens 104-107 19098381-10 2008 High-dose fluvastatin decreased Akt phosphorylation (Ser-473) and HUVEC proliferation, and it increased p27(kip1) in HUVECs. Fluvastatin 10-21 cyclin dependent kinase inhibitor 1B Homo sapiens 108-112 19098381-12 2008 Our data therefore indicate that the stimulatory effects of low-dose fluvastatin on the HGF-induced angiogenesis are mediated by its inhibitory effects on p38 MAPK phosphorylation induced by HGF, which may result in the suppression of EC apoptosis. Fluvastatin 69-80 hepatocyte growth factor Homo sapiens 88-91 19098381-12 2008 Our data therefore indicate that the stimulatory effects of low-dose fluvastatin on the HGF-induced angiogenesis are mediated by its inhibitory effects on p38 MAPK phosphorylation induced by HGF, which may result in the suppression of EC apoptosis. Fluvastatin 69-80 mitogen-activated protein kinase 14 Homo sapiens 155-158 19098381-12 2008 Our data therefore indicate that the stimulatory effects of low-dose fluvastatin on the HGF-induced angiogenesis are mediated by its inhibitory effects on p38 MAPK phosphorylation induced by HGF, which may result in the suppression of EC apoptosis. Fluvastatin 69-80 hepatocyte growth factor Homo sapiens 191-194 19098381-13 2008 High-dose fluvastatin inhibits Akt phosphorylation and HUVEC proliferation, and it increases p27(kip1), which may result in its inhibitory effects on angiogenesis. Fluvastatin 10-21 interferon alpha inducible protein 27 Homo sapiens 93-96 19098381-13 2008 High-dose fluvastatin inhibits Akt phosphorylation and HUVEC proliferation, and it increases p27(kip1), which may result in its inhibitory effects on angiogenesis. Fluvastatin 10-21 cyclin dependent kinase inhibitor 1B Homo sapiens 97-101 18611343-0 2008 [Effects of fluvastatin on the expression of Janus kinase 2/signal transducers and activators of transcription (JAK/STAT) in glomerular mesangial cells under high concentration of glucose]. Fluvastatin 12-23 Janus kinase 2 Rattus norvegicus 45-59 18556704-7 2008 Functionally we demonstrated that fluvastatin could protect macrophages from hypoxia-induced cell death through GRP78 induction. Fluvastatin 34-45 heat shock protein family A (Hsp70) member 5 Homo sapiens 112-117 18628479-6 2008 In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Fluvastatin 13-24 mechanistic target of rapamycin kinase Homo sapiens 36-40 18628479-6 2008 In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Fluvastatin 13-24 eukaryotic translation initiation factor 4E Homo sapiens 111-142 18628479-6 2008 In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Fluvastatin 13-24 eukaryotic translation initiation factor 4E Homo sapiens 144-149 18628479-6 2008 In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Fluvastatin 13-24 eukaryotic translation initiation factor 4E Homo sapiens 196-201 18628479-6 2008 In addition, fluvastatin blocks the mTOR-dependent phosphorylation/deactivation of the translational repressor eukaryotic initiation factor 4E (eIF4E)-binding protein, leading to the formation of eIF4E-binding protein-eIF4E complexes that suppress initiation of cap-dependent mRNA translation. Fluvastatin 13-24 eukaryotic translation initiation factor 4E Homo sapiens 196-201 18628479-7 2008 Importantly, inhibition of p70 S6 kinase activity by fluvastatin results in the up-regulation of expression of programmed cell death 4 (PDCD4), a tumor suppressor protein with inhibitory effects on the translation initiation factor eIF4A, suggesting a mechanism for the generation of antitumor responses. Fluvastatin 53-64 programmed cell death 4 Homo sapiens 111-134 18628479-7 2008 Importantly, inhibition of p70 S6 kinase activity by fluvastatin results in the up-regulation of expression of programmed cell death 4 (PDCD4), a tumor suppressor protein with inhibitory effects on the translation initiation factor eIF4A, suggesting a mechanism for the generation of antitumor responses. Fluvastatin 53-64 programmed cell death 4 Homo sapiens 136-141 18628479-7 2008 Importantly, inhibition of p70 S6 kinase activity by fluvastatin results in the up-regulation of expression of programmed cell death 4 (PDCD4), a tumor suppressor protein with inhibitory effects on the translation initiation factor eIF4A, suggesting a mechanism for the generation of antitumor responses. Fluvastatin 53-64 eukaryotic translation initiation factor 4A1 Homo sapiens 232-237 18628479-8 2008 CONCLUSIONS: Altogether, our findings establish that fluvastatin exhibits potent anti-RCC activities via inhibitory effects on the Akt/mTOR pathway and raise the possibility that combinations of statins and Akt inhibitors may be of future therapeutic value in the treatment of RCC. Fluvastatin 53-64 AKT serine/threonine kinase 1 Homo sapiens 131-134 18628479-8 2008 CONCLUSIONS: Altogether, our findings establish that fluvastatin exhibits potent anti-RCC activities via inhibitory effects on the Akt/mTOR pathway and raise the possibility that combinations of statins and Akt inhibitors may be of future therapeutic value in the treatment of RCC. Fluvastatin 53-64 mechanistic target of rapamycin kinase Homo sapiens 135-139 18628479-8 2008 CONCLUSIONS: Altogether, our findings establish that fluvastatin exhibits potent anti-RCC activities via inhibitory effects on the Akt/mTOR pathway and raise the possibility that combinations of statins and Akt inhibitors may be of future therapeutic value in the treatment of RCC. Fluvastatin 53-64 AKT serine/threonine kinase 1 Homo sapiens 207-210 18846345-8 2008 This experiment suggested that NO-Fluvastatin could suppress the proliferation of HLECs by regulating cell cycle regulatory proteins (inhibiting the expression of CyclinE mRNA and inducing the expression of P21(waf1) mRNA), resulting in the arrest of HLECs in the G(0)/G(1) phase, which can offer theory basis for NO-Fluvastatin in treating posterior capsular opacification in clinic practice. Fluvastatin 34-45 cyclin dependent kinase inhibitor 1A Homo sapiens 207-215 18781850-0 2008 Association between a frequent allele of the gene encoding OATP1B1 and enhanced LDL-lowering response to fluvastatin therapy. Fluvastatin 105-116 solute carrier organic anion transporter family member 1B1 Homo sapiens 59-66 18781850-2 2008 The organic anion transporting polypeptide-1B1 encoded by the SLCO1B1 gene is implicated as a major transporter in cellular uptake of statins, and notably fluvastatin. Fluvastatin 155-166 solute carrier organic anion transporter family member 1B1 Homo sapiens 62-69 18781850-8 2008 CONCLUSIONS: These results reveal that OATP1B1 is implicated in the pharmacological action and efficacy of fluvastatin. Fluvastatin 107-118 solute carrier organic anion transporter family member 1B1 Homo sapiens 39-46 18413661-0 2008 Fluvastatin synergistically improves the antiproliferative effect of everolimus on rat smooth muscle cells by altering p27Kip1/cyclin E expression. Fluvastatin 0-11 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 119-126 18413661-0 2008 Fluvastatin synergistically improves the antiproliferative effect of everolimus on rat smooth muscle cells by altering p27Kip1/cyclin E expression. Fluvastatin 0-11 cyclin E1 Rattus norvegicus 127-135 18413661-8 2008 Taken together, these results demonstrated that everolimus acts synergistically with fluvastatin to inhibit SMC proliferation by altering the expression of cyclin E and p27(kip1), which affects Rb phosphorylation and leads to G(1) phase arrest. Fluvastatin 85-96 cyclin E1 Rattus norvegicus 156-164 18413661-8 2008 Taken together, these results demonstrated that everolimus acts synergistically with fluvastatin to inhibit SMC proliferation by altering the expression of cyclin E and p27(kip1), which affects Rb phosphorylation and leads to G(1) phase arrest. Fluvastatin 85-96 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 169-172 18413661-8 2008 Taken together, these results demonstrated that everolimus acts synergistically with fluvastatin to inhibit SMC proliferation by altering the expression of cyclin E and p27(kip1), which affects Rb phosphorylation and leads to G(1) phase arrest. Fluvastatin 85-96 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 173-177 18611343-1 2008 OBJECTIVE: To investigate the effects of fluvastatin on activation of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 1, 3 (STAT1, 3) in glomerular mesangial cells(GMCs) under high concentration of glucose. Fluvastatin 41-52 Janus kinase 2 Rattus norvegicus 70-84 18611343-1 2008 OBJECTIVE: To investigate the effects of fluvastatin on activation of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 1, 3 (STAT1, 3) in glomerular mesangial cells(GMCs) under high concentration of glucose. Fluvastatin 41-52 Janus kinase 2 Rattus norvegicus 86-90 18611343-1 2008 OBJECTIVE: To investigate the effects of fluvastatin on activation of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 1, 3 (STAT1, 3) in glomerular mesangial cells(GMCs) under high concentration of glucose. Fluvastatin 41-52 signal transducer and activator of transcription 1 Rattus norvegicus 96-161 18611343-9 2008 The concentration of TGF-beta1 [(1.94+/-0.27) microg/L] and FN [(4.27+/-0.33)mg/L] in the supernatants in fluvastatin group were lower than those in high glucose control group (all P<0.05). Fluvastatin 106-117 transforming growth factor, beta 1 Rattus norvegicus 21-30 18611343-10 2008 CONCLUSION: Fluvastatin can inhibit overproduction of TGF-beta1 and FN in GMCs under high concentration of glucose, the underlying mechanism may partly be attributable to its influence on phosphorylation of JAK/STAT. Fluvastatin 12-23 transforming growth factor, beta 1 Rattus norvegicus 54-63 18452779-0 2008 Effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, fluvastatin, on coronary spasm after withdrawal of calcium-channel blockers. Fluvastatin 72-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 13-60 18430418-0 2008 Fluvastatin decreases cardiac fibrosis possibly through regulation of TGF-beta(1)/Smad 7 expression in the spontaneously hypertensive rats. Fluvastatin 0-11 transforming growth factor, beta 1 Rattus norvegicus 70-81 18430418-0 2008 Fluvastatin decreases cardiac fibrosis possibly through regulation of TGF-beta(1)/Smad 7 expression in the spontaneously hypertensive rats. Fluvastatin 0-11 SMAD family member 7 Rattus norvegicus 82-88 18430418-8 2008 For example, the hydroxyproline content was 3.2+/-0.1, 4.0+/-0.1 and 3.5+/-0.1 microg/mg heart and the Smad 7 protein expression was 5.1+/-0.6, 1.0+/-0.1 and 4.1+/-0.7 arbitrary units for WKY rats, SHRs and SHRs receiving 20 mg/kg/day fluvastatin, respectively. Fluvastatin 235-246 SMAD family member 7 Rattus norvegicus 103-109 18430418-9 2008 The hydroxyproline content in the SHRs treated with or without fluvastatin was positively correlated with the left ventricular mass index, systolic blood pressure and the amount of TGF-beta1 proteins and negatively correlated with the Smad 7 expression level. Fluvastatin 63-74 transforming growth factor, beta 1 Rattus norvegicus 181-190 18430418-9 2008 The hydroxyproline content in the SHRs treated with or without fluvastatin was positively correlated with the left ventricular mass index, systolic blood pressure and the amount of TGF-beta1 proteins and negatively correlated with the Smad 7 expression level. Fluvastatin 63-74 SMAD family member 7 Rattus norvegicus 235-241 18384769-1 2008 The present study was designed to investigate whether fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, would attenuate the acute myocardial infarction in isoproterenol-treated rat model via maintaining activities of endogenous antioxidant enzymes. Fluvastatin 54-65 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 69-126 18221360-0 2008 Fluvastatin reduces oxidative damage in human vascular endothelial cells by upregulating Bcl-2. Fluvastatin 0-11 BCL2 apoptosis regulator Homo sapiens 89-94 18308946-7 2008 In vitro mono-treatment with either fluvastatin (100 nM) or SDF-1 (100 ng/ml) facilitated EPC proliferation and migration, inhibited EPC apoptosis, enhanced expression of matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9), and increased Akt phosphorylation and nitric oxide production. Fluvastatin 36-47 matrix metallopeptidase 2 Mus musculus 171-197 18308946-7 2008 In vitro mono-treatment with either fluvastatin (100 nM) or SDF-1 (100 ng/ml) facilitated EPC proliferation and migration, inhibited EPC apoptosis, enhanced expression of matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9), and increased Akt phosphorylation and nitric oxide production. Fluvastatin 36-47 matrix metallopeptidase 2 Mus musculus 199-212 18308946-7 2008 In vitro mono-treatment with either fluvastatin (100 nM) or SDF-1 (100 ng/ml) facilitated EPC proliferation and migration, inhibited EPC apoptosis, enhanced expression of matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9), and increased Akt phosphorylation and nitric oxide production. Fluvastatin 36-47 matrix metallopeptidase 9 Mus musculus 214-219 18308946-7 2008 In vitro mono-treatment with either fluvastatin (100 nM) or SDF-1 (100 ng/ml) facilitated EPC proliferation and migration, inhibited EPC apoptosis, enhanced expression of matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9), and increased Akt phosphorylation and nitric oxide production. Fluvastatin 36-47 thymoma viral proto-oncogene 1 Mus musculus 236-239 18065496-4 2008 In our current study, we show that simvastatin, pravastatin and fluvastatin can induce PTEN expression in a dose-dependent manner. Fluvastatin 64-75 phosphatase and tensin homolog Homo sapiens 87-91 18221360-6 2008 The protective effect of fluvastatin was mediated by the upregulation of Bcl-2 expression as probed by real-time polymerase chain reaction and Western blotting. Fluvastatin 25-36 BCL2 apoptosis regulator Homo sapiens 73-78 18221360-7 2008 Using siRNA to knock down the expression of Bcl-2, the protective effect of fluvastatin was abolished. Fluvastatin 76-87 BCL2 apoptosis regulator Homo sapiens 44-49 18221360-9 2008 CONCLUSIONS: These results suggest that fluvastatin has a potent protective effect against H(2)O(2)-induced apoptosis via upregulation of Bcl-2 expression. Fluvastatin 40-51 BCL2 apoptosis regulator Homo sapiens 138-143 18343245-12 2008 NCEP ATP III LDL-C goals were achieved by 87% of patients receiving fluvastatin XL + ezetimibe and 67% of patients receiving fluvastatin XL monotherapy (between-group difference, P = 0.042). Fluvastatin 68-79 component of oligomeric golgi complex 2 Homo sapiens 13-18 19099972-12 2008 IFN-gamma further increased PBMNC CD40 expressions in all subjects after culturing for 24 h and fluvastatin equally inhibited IFN-gamma induced PBMNC CD40 expression from various genotypes (CC, CT, TT was 30.3%, 26.3%, 29.3% respectively, all P > 0.05). Fluvastatin 96-107 interferon gamma Homo sapiens 126-135 19099972-12 2008 IFN-gamma further increased PBMNC CD40 expressions in all subjects after culturing for 24 h and fluvastatin equally inhibited IFN-gamma induced PBMNC CD40 expression from various genotypes (CC, CT, TT was 30.3%, 26.3%, 29.3% respectively, all P > 0.05). Fluvastatin 96-107 CD40 molecule Homo sapiens 150-154 17905618-4 2008 The affinity for BLG increased in the sequence: 5-fluorosalycilic acid<dexamethasone<<sulindac=norfloxacin<fluvastatin. Fluvastatin 119-130 beta-lactoglobulin Bos taurus 17-20 17905618-6 2008 Conversely, the Ki for fluvastatin and norfloxacin were in the order of 10(-7) and 10(-6)M, similar to the affinity for BLG by natural ligands, such as retinoids and long-chain fatty acids. Fluvastatin 23-34 beta-lactoglobulin Bos taurus 120-123 17905618-8 2008 Interaction of fluvastatin and norfloxacin with BLG was made evident by changes in chemical shift and dynamic parameters in the 19F NMR spectra and in effective urea concentration and cooperativity features in denaturant gradient gel electrophoresis. Fluvastatin 15-26 beta-lactoglobulin Bos taurus 48-51 18343245-5 2008 The primary end point was the percentage change from baseline to week 12 in LDL-C level with fluvastatin XL + ezetimibe combination therapy compared with fluvastatin XL alone. Fluvastatin 93-104 component of oligomeric golgi complex 2 Homo sapiens 76-81 17383753-0 2008 Fluvastatin reduces increased blood monocyte Toll-like receptor 4 expression in whole blood from patients with chronic heart failure. Fluvastatin 0-11 toll like receptor 4 Homo sapiens 45-65 17383753-9 2008 Pre-incubation with fluvastatin for 24 h inhibited dose-dependently ex vivo monocyte TLR4 and TLR2 expressions (p<0.001). Fluvastatin 20-31 toll like receptor 4 Homo sapiens 85-89 17383753-9 2008 Pre-incubation with fluvastatin for 24 h inhibited dose-dependently ex vivo monocyte TLR4 and TLR2 expressions (p<0.001). Fluvastatin 20-31 toll like receptor 2 Homo sapiens 94-98 18176067-0 2008 [Fluvastatin induces apoptosis on human tongue carcinoma cell line HSC-3]. Fluvastatin 1-12 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 67-72 18176067-3 2008 In this study, we investigated the mechanism by which fluvastatin induces apoptosis in HSC-3 cells. Fluvastatin 54-65 DnaJ heat shock protein family (Hsp40) member B7 Homo sapiens 87-92 18176067-6 2008 When we examined the survival signals at the time of apoptotic induction, we also found that fluvastatin had caused a remarkable decrease in the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Fluvastatin 93-104 mitogen-activated protein kinase 3 Homo sapiens 164-211 18176067-8 2008 These results suggested that fluvastatin induces apoptosis by inhibiting GGPP biosynthesis and consequently decreasing the level of phosphorylated ERK1/2. Fluvastatin 29-40 mitogen-activated protein kinase 3 Homo sapiens 147-153 17919370-0 2007 Effect of fluvastatin on vascular endothelial growth factor in rats with osteoporosis in process of fracture healing. Fluvastatin 10-21 vascular endothelial growth factor A Rattus norvegicus 25-59 18031608-10 2007 Treatment with fluvastatin reduced phosphorylation levels of JAK2, STAT1, STAT3, and SHP-2 in glomeruli of diabetic rats, but it had no effect on the dephosphorylation of SHP-1. Fluvastatin 15-26 Janus kinase 2 Rattus norvegicus 61-65 18031608-10 2007 Treatment with fluvastatin reduced phosphorylation levels of JAK2, STAT1, STAT3, and SHP-2 in glomeruli of diabetic rats, but it had no effect on the dephosphorylation of SHP-1. Fluvastatin 15-26 signal transducer and activator of transcription 1 Rattus norvegicus 67-72 18031608-10 2007 Treatment with fluvastatin reduced phosphorylation levels of JAK2, STAT1, STAT3, and SHP-2 in glomeruli of diabetic rats, but it had no effect on the dephosphorylation of SHP-1. Fluvastatin 15-26 signal transducer and activator of transcription 3 Rattus norvegicus 74-79 18031608-10 2007 Treatment with fluvastatin reduced phosphorylation levels of JAK2, STAT1, STAT3, and SHP-2 in glomeruli of diabetic rats, but it had no effect on the dephosphorylation of SHP-1. Fluvastatin 15-26 protein tyrosine phosphatase, non-receptor type 11 Rattus norvegicus 85-90 17324434-9 2007 Fluvastatin, a drug known to improve endothelial function, was shown to prevent OSS up-regulation of the ppET-1 gene expression. Fluvastatin 0-11 endothelin 1 Bos taurus 105-111 17324434-10 2007 Under this flow condition, fluvastatin affects ppET-1 gene expression via inhibition of its promoter activity without affecting ppET-1mRNA stability. Fluvastatin 27-38 endothelin 1 Bos taurus 47-53 17324434-12 2007 The transcriptional up-regulation of ppET-1 was shown to be fluvastatin sensitive. Fluvastatin 60-71 endothelin 1 Bos taurus 37-43 17975105-8 2007 Consistently, BrdU/CD31-positive cells were significantly increased in fluvastatin-treated rats after 7 days of treatment. Fluvastatin 71-82 platelet and endothelial cell adhesion molecule 1 Rattus norvegicus 19-23 17975105-9 2007 MAP1B-positive neurites were also increased in the peri-infarct region in fluvastatin-treated rats. Fluvastatin 74-85 microtubule-associated protein 1B Rattus norvegicus 0-5 17975105-10 2007 In addition, rats treated with fluvastatin showed the reduction of superoxide anion after 7 days of treatment and the reduction of A beta deposits in the thalamic nuclei after 3 months of treatment. Fluvastatin 31-42 amyloid beta precursor protein Rattus norvegicus 131-137 17975105-12 2007 Pleiotropic effects of fluvastatin, such as angiogenesis, neuritogenesis, and inhibition of superoxide production and A beta deposition, might be associated with a favorable outcome. Fluvastatin 23-34 amyloid beta precursor protein Rattus norvegicus 118-124 17878231-5 2007 Conversely, cholesterol-lowering agents (fluvastatin and lovastatin) and cholesterol-depleting agents (beta-cyclodextrin and nystatin) enhance TGF-beta responsiveness by increasing non-lipid raft microdomain accumulation of TGF-beta receptors and facilitating TGF-beta-induced signaling. Fluvastatin 41-52 transforming growth factor, beta 1 Mus musculus 143-151 17556673-0 2007 Fluvastatin inhibits hypoxic proliferation and p38 MAPK activity in pulmonary artery fibroblasts. Fluvastatin 0-11 mitogen-activated protein kinase 14 Homo sapiens 47-50 17919370-1 2007 OBJECTIVE: To explore the effect of fluvastatin on vascular endothelial growth factor (VEGF) in rats with osteoporosis in the process of fracture healing. Fluvastatin 36-47 vascular endothelial growth factor A Rattus norvegicus 51-85 17919370-1 2007 OBJECTIVE: To explore the effect of fluvastatin on vascular endothelial growth factor (VEGF) in rats with osteoporosis in the process of fracture healing. Fluvastatin 36-47 vascular endothelial growth factor A Rattus norvegicus 87-91 17919370-7 2007 CONCLUSION: Fluvastatin can promote the VEGF level in rats with osteoporosis in process of fracture healing. Fluvastatin 12-23 vascular endothelial growth factor A Rattus norvegicus 40-44 17472573-0 2007 Fluvastatin inhibits regulated secretion of endothelial cell von Willebrand factor in response to diverse secretagogues. Fluvastatin 0-11 von Willebrand factor Homo sapiens 61-82 17563401-6 2007 Polymorphisms in 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) previously reported to affect the efficacy of pravastatin did not show a similar effect on the reduction of LDL cholesterol by fluvastatin. Fluvastatin 200-211 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 66-71 17472573-4 2007 We studied the effect of fluvastatin on regulated secretion of vWF from HUVEC (human umbilical-vein ECs). Fluvastatin 25-36 von Willebrand factor Homo sapiens 63-66 17470528-0 2007 Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3. Fluvastatin 64-75 solute carrier organic anion transporter family member 1B1 Homo sapiens 142-149 17472573-9 2007 Fluvastatin increased eNOS [endothelial NOS (NO synthase)] expression, but NOS inhibitors failed to reverse the effect of fluvastatin on vWF secretion. Fluvastatin 0-11 nitric oxide synthase 3 Homo sapiens 22-26 17470528-0 2007 Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3. Fluvastatin 64-75 solute carrier organic anion transporter family member 2B1 Homo sapiens 151-158 17472573-14 2007 We conclude that, via inhibition of protein geranylgeranylation, fluvastatin is a broadspectrum inhibitor of regulated vWF secretion. Fluvastatin 65-76 von Willebrand factor Homo sapiens 119-122 17470528-0 2007 Substrate-dependent drug-drug interactions between gemfibrozil, fluvastatin and other organic anion-transporting peptide (OATP) substrates on OATP1B1, OATP2B1, and OATP1B3. Fluvastatin 64-75 solute carrier organic anion transporter family member 1B3 Homo sapiens 164-171 17472573-15 2007 Geranylgeranylated small GTPases with functional roles in regulated secretion, such as Cdc42, are potential targets for the inhibitory activity of fluvastatin. Fluvastatin 147-158 cell division cycle 42 Homo sapiens 87-92 17470528-5 2007 For OATP1B1 the inhibition by gemfibrozil was substrate-dependent as the transport of fluvastatin (IC(50) of 63 microM), pravastatin, simvastatin, and taurocholate was inhibited by gemfibrozil, whereas the transport of estrone-3-sulfate and troglitazone sulfate (both used at 3 microM) was not affected. Fluvastatin 86-97 solute carrier organic anion transporter family member 1B1 Homo sapiens 4-11 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 53-64 solute carrier organic anion transporter family member 1B1 Homo sapiens 12-19 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 221-232 solute carrier organic anion transporter family member 1B1 Homo sapiens 12-19 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 53-64 solute carrier organic anion transporter family member 2B1 Homo sapiens 22-29 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 53-64 solute carrier organic anion transporter family member 1B3 Homo sapiens 36-43 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 221-232 solute carrier organic anion transporter family member 2B1 Homo sapiens 22-29 17470528-8 2007 Recombinant OATP1B1-, OATP2B1-, and OATP1B3-mediated fluvastatin transport was inhibited to 97, 70, and 62% by gemfibrozil (200 microM), respectively, whereas only a small inhibitory effect by gemfibrozil (200 microM) on fluvastatin uptake into primary human hepatocytes was observed (27% inhibition). Fluvastatin 221-232 solute carrier organic anion transporter family member 1B3 Homo sapiens 36-43 17004104-11 2007 Rapamycin, an inhibitor of MTOR, was synergistic with fluvastatin in two of the four cell lines and antagonistic in two other cell lines. Fluvastatin 54-65 mechanistic target of rapamycin kinase Homo sapiens 27-31 17466485-0 2007 Simvastatin and fluvastatin reduce interleukin-6 and interleukin-8 lipopolysaccharide (LPS) stimulated production by isolated human monocytes from chronic kidney disease patients. Fluvastatin 16-27 interleukin 6 Homo sapiens 35-48 17466485-0 2007 Simvastatin and fluvastatin reduce interleukin-6 and interleukin-8 lipopolysaccharide (LPS) stimulated production by isolated human monocytes from chronic kidney disease patients. Fluvastatin 16-27 C-X-C motif chemokine ligand 8 Homo sapiens 53-66 17671209-10 2007 Both fluvastatin and simvastatin increased iNOS mRNA and protein expression. Fluvastatin 5-16 nitric oxide synthase 2 Homo sapiens 43-47 17004104-12 2007 The combination of fluvastatin or another inhibitor of prenylation and trastuzumab may be attractive for clinical development as the effect of trastuzumab in Her2/neu positive breast tumors is incomplete as a single agent. Fluvastatin 19-30 erb-b2 receptor tyrosine kinase 2 Homo sapiens 158-162 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 selectin P Homo sapiens 36-46 17615423-12 2007 In patients requiring the concurrent use of statins and CYP3A4 inhibitors, pravastatin, fluvastatin, and rosuvastatin carry the lowest risk of drug interactions; atorvastatin carries moderate risk, whereas simvastatin and lovastatin have the highest risk and should be avoided in patients taking concomitant CYP3A4 inhibitors. Fluvastatin 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 56-62 17615423-12 2007 In patients requiring the concurrent use of statins and CYP3A4 inhibitors, pravastatin, fluvastatin, and rosuvastatin carry the lowest risk of drug interactions; atorvastatin carries moderate risk, whereas simvastatin and lovastatin have the highest risk and should be avoided in patients taking concomitant CYP3A4 inhibitors. Fluvastatin 88-99 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 308-314 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 serpin family E member 1 Homo sapiens 48-53 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 plasminogen activator, tissue type Homo sapiens 59-63 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 selectin P Homo sapiens 223-233 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 serpin family E member 1 Homo sapiens 242-247 17666915-11 2007 The postprandial increase in plasma P-selectin, PAI-1, and t-PA antigen levels was attenuated by 1-week fluvastatin-alone and valsartan-alone treatments; their combination is more effective on both fasting and postprandial P-selectin, plasma PAI-1, and t-PA antigen levels. Fluvastatin 104-115 plasminogen activator, tissue type Homo sapiens 253-257 17353078-8 2007 Pretreatment of test rats with fluvastatin decreased blood levels of certain markers of organ injury, suppressed the release of TNF-alpha and increased IL-10, and NO levels following LPS treatment. Fluvastatin 31-42 tumor necrosis factor Rattus norvegicus 128-137 17353078-8 2007 Pretreatment of test rats with fluvastatin decreased blood levels of certain markers of organ injury, suppressed the release of TNF-alpha and increased IL-10, and NO levels following LPS treatment. Fluvastatin 31-42 interleukin 10 Rattus norvegicus 152-157 17353078-10 2007 CONCLUSIONS: Pre-treatment with fluvastatin suppresses the release of plasma TNF-alpha, increases plasma IL-10, and NO production, and decreases the levels of markers of organ injury associated with endotoxic shock, so ameliorating LPS-induced organ damage amongst conscious rats. Fluvastatin 32-43 tumor necrosis factor Rattus norvegicus 77-86 17353078-10 2007 CONCLUSIONS: Pre-treatment with fluvastatin suppresses the release of plasma TNF-alpha, increases plasma IL-10, and NO production, and decreases the levels of markers of organ injury associated with endotoxic shock, so ameliorating LPS-induced organ damage amongst conscious rats. Fluvastatin 32-43 interleukin 10 Rattus norvegicus 105-110 17264303-2 2007 Exposure of U937 and U266 cells to minimally toxic concentrations of UCN-01 and various statins (eg, lovastatin, simvastatin, or fluvastatin) dramatically increased mitochondrial dysfunction, caspase activation, and apoptosis. Fluvastatin 129-140 urocortin Homo sapiens 69-72 17379842-0 2007 Fluvastatin alters platelet aggregability in patients with hypercholesterolemia: possible improvement of intraplatelet redox imbalance via HMG-CoA reductase. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 139-156 17530711-11 2007 Fluvastatin decreased the levels of expression of messenger RNA for p22phox, a NAD(P)H oxidase component, in the aortas of rats with AIA, but did not affect the expression of eNOS. Fluvastatin 0-11 cytochrome b-245 alpha chain Rattus norvegicus 68-75 17289397-0 2007 Tolerability of statins is not linked to CYP450 polymorphisms, but reduced CYP2D6 metabolism improves cholesteraemic response to simvastatin and fluvastatin. Fluvastatin 145-156 cytochrome P450 family 2 subfamily D member 6 Homo sapiens 75-81 17513950-10 2007 After 96 hours of treatment, fluvastatin and lovastatin clearly increased CYP2C9 protein level. Fluvastatin 29-40 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 74-80 17307149-2 2007 In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach. Fluvastatin 258-264 cytochrome P450 family 2 subfamily C member 19 Homo sapiens 95-102 17307149-2 2007 In order to gain insights for developing personalized drugs, the 3D (dimensional) structure of CYP2C19 has been developed based on the crystal structure of CYP2C9 (PDB code 1R90), and its structure-activity relationship with the ligands of CEC, Fluvoxamine, Lescol, and Ticlopidine investigated through the structure-activity relationship approach. Fluvastatin 258-264 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 156-162 17416287-0 2007 Effect of paraoxonase 1 polymorphisms on the response of lipids and lipoprotein-associated enzymes to treatment with fluvastatin. Fluvastatin 117-128 paraoxonase 1 Homo sapiens 10-23 17416287-6 2007 RESULTS: Fluvastatin treatment did not affect HDL-cholesterol or apolipoprotein (apo) AI but resulted in significant decreases in total cholesterol, triglycerides, low-density lipoprotein-cholesterol, apo B and apo E, as well as total serum Lp-PLA(2) activity. Fluvastatin 9-20 apolipoprotein E Homo sapiens 211-216 17416287-6 2007 RESULTS: Fluvastatin treatment did not affect HDL-cholesterol or apolipoprotein (apo) AI but resulted in significant decreases in total cholesterol, triglycerides, low-density lipoprotein-cholesterol, apo B and apo E, as well as total serum Lp-PLA(2) activity. Fluvastatin 9-20 phospholipase A2 group VII Homo sapiens 241-250 17560160-11 2007 Mevalonate cycle inhibiting fluvastatin and 25-hydroxycholesterol decreased cholesterol production in leptin-stimulated monocytes. Fluvastatin 28-39 leptin Homo sapiens 102-108 17341842-5 2007 Pravastatin and fluvastatin significantly (P<0.05) decreased MPO activities, but only pravastatin decreased the incidence of ischemia-induced lethal VF. Fluvastatin 16-27 myeloperoxidase Rattus norvegicus 64-67 17446458-3 2007 We found that fluvastatin, an HMG-CoA reductase inhibitor, decreased NCX1 mRNA and protein by inhibiting a small G protein, RhoB, in H9c2 cardiomyoblasts. Fluvastatin 14-25 solute carrier family 8 member A1 Homo sapiens 69-73 17446458-3 2007 We found that fluvastatin, an HMG-CoA reductase inhibitor, decreased NCX1 mRNA and protein by inhibiting a small G protein, RhoB, in H9c2 cardiomyoblasts. Fluvastatin 14-25 ras homolog family member B Homo sapiens 124-128 17182966-4 2007 Two lipophilic statins (simvastatin and fluvastatin) suppressed the cytotoxic activity of fresh and IL-2-stimulated NK cells, while pravastatin, a hydrophilic statin, did not. Fluvastatin 40-51 interleukin 2 Homo sapiens 100-104 18688288-5 2007 When the release of fluvastatin was controlled to occur over 2 weeks, BMP2 and ALP production was increased 2.2-fold and 1.7-fold, respectively, at day 28 compared to hMSCs cultured in the absence of fluvastatin. Fluvastatin 20-31 bone morphogenetic protein 2 Homo sapiens 70-74 18688288-5 2007 When the release of fluvastatin was controlled to occur over 2 weeks, BMP2 and ALP production was increased 2.2-fold and 1.7-fold, respectively, at day 28 compared to hMSCs cultured in the absence of fluvastatin. Fluvastatin 20-31 alkaline phosphatase, placental Homo sapiens 79-82 18688288-6 2007 By introducing a heparin functionality into the gel to sequester and localize the hMSC-produced BMP2, the osteogenic differentiation of hMSCs was further augmented over fluvastatin delivery alone. Fluvastatin 169-180 bone morphogenetic protein 2 Homo sapiens 96-100 18688288-7 2007 Osteopontin and core binding factor alpha1 gene expression was 6-fold and 4-fold greater for hMSCs exposed to fluvastatin in the presence of the heparin functionalities, respectively. Fluvastatin 110-121 secreted phosphoprotein 1 Homo sapiens 0-11 16860387-6 2006 Released fluvastatin increased human mesenchymal stem cell (hMSC) gene expression of CBFA1, ALP, and COL I by 34-fold, 2.6-fold, and 1.8-fold, respectively, after 14 days of in vitro culture. Fluvastatin 9-20 RUNX family transcription factor 2 Homo sapiens 85-90 16860387-6 2006 Released fluvastatin increased human mesenchymal stem cell (hMSC) gene expression of CBFA1, ALP, and COL I by 34-fold, 2.6-fold, and 1.8-fold, respectively, after 14 days of in vitro culture. Fluvastatin 9-20 ATHS Homo sapiens 92-95 16860387-7 2006 In addition, treating hMSCs with the released fluvastatin resulted in an average of 2.0- and 1.5-fold greater BMP2 production whereas mineralization increased an average of 3.0-fold and 2.5-fold for 0.01 and 0.1 microM fluvastatin, respectively, over the 2 week culture period. Fluvastatin 46-57 bone morphogenetic protein 2 Homo sapiens 110-114 17178259-6 2006 Cerivastatin is metabolized by CYP2C8 and CYP3A4, and fluvastatin is metabolized by CYP2C9. Fluvastatin 54-65 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 84-90 17031388-10 2006 Either fluvastatin (at both doses) or atorvastatin reduced sarcolemma gCl and changed MT. Fluvastatin 7-18 germ cell-less 1, spermatogenesis associated Rattus norvegicus 70-73 17178259-7 2006 The exposure to fluvastatin is increased by less than 2-fold by inhibitors of CYP2C9. Fluvastatin 16-27 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 78-84 17003232-0 2006 Phosphorylation of endothelial nitric-oxide synthase is diminished in mesenteric arteries from septic rabbits depending on the altered phosphatidylinositol 3-kinase/Akt pathway: reversal effect of fluvastatin therapy. Fluvastatin 197-208 nitric oxide synthase, endothelial Oryctolagus cuniculus 19-52 17164750-3 2006 The aim of this study was to establish the effect of a 3-month treatment of fluvastatin on circulating (c)ICAM-1 and standard lipid parameters. Fluvastatin 76-87 intercellular adhesion molecule 1 Homo sapiens 106-112 17003232-7 2006 In vivo treatment with fluvastatin restored the decrease in eNOS phosphorylation in septic mesenteric vessels. Fluvastatin 23-34 nitric oxide synthase, endothelial Oryctolagus cuniculus 60-64 17003232-9 2006 Treatment with the PI3-K inhibitor wortmannin partially inhibited the fluvastatin-induced increases in phosphorylation of Akt and eNOS, and the decrease in translocation of PI3-K heterodimer to the membranes during sepsis was slightly improved by fluvastatin. Fluvastatin 70-81 nitric oxide synthase, endothelial Oryctolagus cuniculus 130-134 17003232-10 2006 Sepsis-induced impairment of eNOS expression was also nearly normalized by fluvastatin. Fluvastatin 75-86 nitric oxide synthase, endothelial Oryctolagus cuniculus 29-33 17003232-13 2006 We also suggest that fluvastatin would ameliorate vascular endothelial dysfunction, in part, presumably via its recovery effect on Akt-dependent eNOS phosphorylation. Fluvastatin 21-32 nitric oxide synthase, endothelial Oryctolagus cuniculus 145-149 17086097-6 2006 Fluvastatin (0.03%) significantly reduced both LOX-1-ligand and T-CHO. Fluvastatin 0-11 oxidized low-density lipoprotein receptor 1 Oryctolagus cuniculus 47-52 17062478-9 2006 CONCLUSION: Fluvastatin lowered LDL cholesterol, total cholesterol and apolipoprotein B levels effectively over a prolonged period in children and adolescents with heterozygous familial hypercholesterolaemia. Fluvastatin 12-23 apolipoprotein B Homo sapiens 71-87 17015053-1 2006 OBJECTIVE: Pravastatin is a hydrophilic substrate and fluvastatin a lipophilic substrate of the hepatic uptake transporter organic anion transporting polypeptide 1B1 encoded by SLCO1B1. Fluvastatin 54-65 solute carrier organic anion transporter family member 1B1 Homo sapiens 177-184 17015053-2 2006 Our aim was to compare the effects of SLCO1B1 polymorphism on the pharmacokinetics of pravastatin and fluvastatin. Fluvastatin 102-113 solute carrier organic anion transporter family member 1B1 Homo sapiens 38-45 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Fluvastatin 31-42 cyclin dependent kinase 2 Homo sapiens 80-84 16714062-6 2006 Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9. Fluvastatin 114-125 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 100-106 16714062-6 2006 Among the statins, simvastatin, lovastatin and atorvastatin are metabolized by cytochrome P450 3A4 (CYP3A4) while fluvastatin is metabolized by CYP2C9. Fluvastatin 114-125 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 144-150 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Fluvastatin 31-42 cyclin dependent kinase 2 Homo sapiens 244-248 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Fluvastatin 31-42 H3 histone pseudogene 16 Homo sapiens 289-292 16985065-9 2006 All three statins (lovastatin, fluvastatin, and simvastatin) inhibited cyclin E/cdk2 kinase leading to hypophosphorylation of Rb, but this inhibition was correlated with a loss of the activating phosphorylation on Thr160 of cyclin E-associated cdk2 and not dependent on the cdk inhibitors p21 and p27. Fluvastatin 31-42 dynactin subunit 6 Homo sapiens 297-300 16735695-3 2006 Previously, we found that pravastatin, fluvastatin, and simvastatin induced the production of IL-18 in human monocytes. Fluvastatin 39-50 interleukin 18 Homo sapiens 94-99 16895538-9 2006 RhoA, as assessed by western blotting, was also reduced by fluvastatin treatment. Fluvastatin 59-70 ras homolog family member A Rattus norvegicus 0-4 16712874-0 2006 HMG-CoA reductase inhibitor fluvastatin prevents angiotensin II-induced cardiac hypertrophy via Rho kinase and inhibition of cyclin D1. Fluvastatin 28-39 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 0-17 16712874-0 2006 HMG-CoA reductase inhibitor fluvastatin prevents angiotensin II-induced cardiac hypertrophy via Rho kinase and inhibition of cyclin D1. Fluvastatin 28-39 angiotensinogen Rattus norvegicus 49-63 16712874-0 2006 HMG-CoA reductase inhibitor fluvastatin prevents angiotensin II-induced cardiac hypertrophy via Rho kinase and inhibition of cyclin D1. Fluvastatin 28-39 cyclin D1 Rattus norvegicus 125-134 16712874-5 2006 To investigate whether HMG-CoA reductase inhibitors prevent cardiac hypertrophy through attenuation of Rho and cyclin D1, we studied the effect of fluvastatin on angiotensin II-induced cardiomyocyte hypertrophy in vitro and in vivo. Fluvastatin 147-158 angiotensinogen Rattus norvegicus 162-176 16712874-6 2006 Angiotensin II increased the cell surface area and [(3)H]leucine uptake of cultured neonatal rat cardiomyocytes and these changes were suppressed by fluvastatin treatment. Fluvastatin 149-160 angiotensinogen Rattus norvegicus 0-14 16712874-7 2006 Angiotensin II also induced activation of Rho kinase and increased cyclin D1, both of which were also significantly suppressed by fluvastatin. Fluvastatin 130-141 angiotensinogen Rattus norvegicus 0-14 16712874-7 2006 Angiotensin II also induced activation of Rho kinase and increased cyclin D1, both of which were also significantly suppressed by fluvastatin. Fluvastatin 130-141 cyclin D1 Rattus norvegicus 67-76 16712874-9 2006 Overexpression of cyclin D1 by adenoviral gene transfer induced cardiomyocyte hypertrophy, as evidenced by increased cell size and increased protein synthesis; this hypertrophy was not diminished by concomitant treatment with fluvastatin. Fluvastatin 226-237 cyclin D1 Rattus norvegicus 18-27 16712874-10 2006 Infusion of angiotensin II to Wistar rats for 2 weeks induced hypertrophic changes in cardiomyocytes, and this hypertrophy was prevented by oral fluvastatin treatment. Fluvastatin 145-156 angiotensinogen Rattus norvegicus 12-26 16712874-11 2006 These results show that an HMG-CoA reductase inhibitor, fluvastatin, prevents angiotensin II-induced cardiomyocyte hypertrophy in part through inhibition of cyclin D1, which is linked to Rho kinase. Fluvastatin 56-67 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 27-44 16712874-11 2006 These results show that an HMG-CoA reductase inhibitor, fluvastatin, prevents angiotensin II-induced cardiomyocyte hypertrophy in part through inhibition of cyclin D1, which is linked to Rho kinase. Fluvastatin 56-67 angiotensinogen Rattus norvegicus 78-92 16712874-11 2006 These results show that an HMG-CoA reductase inhibitor, fluvastatin, prevents angiotensin II-induced cardiomyocyte hypertrophy in part through inhibition of cyclin D1, which is linked to Rho kinase. Fluvastatin 56-67 cyclin D1 Rattus norvegicus 157-166 16712874-12 2006 This novel mechanism discovered for fluvastatin could be revealed how HMG-CoA reductase inhibitors are preventing cardiac hypertrophy. Fluvastatin 36-47 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 70-87 16735695-4 2006 The addition of mevalonate abolished the IL-18 production induced by pravastatin, fluvastatin, and simvastatin, indicating that the IL-18 production might be a result of the inhibition of HMG-CoA reductase. Fluvastatin 82-93 interleukin 18 Homo sapiens 41-46 16647179-0 2006 Protective effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on copper-induced hydroxyl radical generation in the rat heart. Fluvastatin 21-32 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 50-97 16773203-6 2006 The inhibitory effects of fluvastatin, GGTI-298 and FTI-277 on MDA-MB-231 cell invasion were shown to correlate well with inhibition of the membrane localization of RhoA and RhoC, but not with Ras. Fluvastatin 26-37 ras homolog family member A Homo sapiens 165-169 16773203-6 2006 The inhibitory effects of fluvastatin, GGTI-298 and FTI-277 on MDA-MB-231 cell invasion were shown to correlate well with inhibition of the membrane localization of RhoA and RhoC, but not with Ras. Fluvastatin 26-37 ras homolog family member C Homo sapiens 174-178 16647179-1 2006 The present study was examined the effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on Cu(II)-induced hydroxyl radical generation (OH) in the extracellular fluid of rat myocardium. Fluvastatin 45-56 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 74-131 16618834-6 2006 The average decrease of LDL-c was 1.7+/-0.7 mmol/L after 4 weeks of fluvastatin (P<0.001). Fluvastatin 68-79 component of oligomeric golgi complex 2 Homo sapiens 24-29 16472797-10 2006 CONCLUSION: Early fluvastatin intervention decreases dose-dependently the serum concentrations of hs-CRP and TNF-alpha of patients with ACS. Fluvastatin 18-29 tumor necrosis factor Homo sapiens 109-118 16618834-7 2006 The mean Pd-20 for Ang II increased by 1.28 ng/kg per minute (95% CI, 2.05 to 0.50; P=0.002) on fluvastatin, corresponding with a 26% decrease in Ang II sensitivity. Fluvastatin 96-107 angiotensinogen Homo sapiens 19-25 16874687-0 2006 Fluvastatin prevents oxidized low-density lipoprotein-induced injury of renal tubular epithelial cells by inhibiting the phosphatidylinositol 3-kinase/Akt-signaling pathway. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 151-154 16624629-0 2006 TGF-beta1-induced thrombospondin-1 expression through the p38 MAPK pathway is abolished by fluvastatin in human coronary artery smooth muscle cells. Fluvastatin 91-102 transforming growth factor beta 1 Homo sapiens 0-9 16624629-0 2006 TGF-beta1-induced thrombospondin-1 expression through the p38 MAPK pathway is abolished by fluvastatin in human coronary artery smooth muscle cells. Fluvastatin 91-102 thrombospondin 1 Homo sapiens 18-34 16624629-2 2006 This study evaluated the hypothesis that the HMG-CoA reductase inhibitor fluvastatin inhibits TGF-beta1 induced TSP-1 expression via inhibition of p38 mitogen activated protein kinase (MAPK) phosphorylation in human coronary artery smooth muscle cells (HCASMC) and may therefore have anti-restenosis potential. Fluvastatin 73-84 transforming growth factor beta 1 Homo sapiens 94-103 16624629-2 2006 This study evaluated the hypothesis that the HMG-CoA reductase inhibitor fluvastatin inhibits TGF-beta1 induced TSP-1 expression via inhibition of p38 mitogen activated protein kinase (MAPK) phosphorylation in human coronary artery smooth muscle cells (HCASMC) and may therefore have anti-restenosis potential. Fluvastatin 73-84 thrombospondin 1 Homo sapiens 112-117 16624629-2 2006 This study evaluated the hypothesis that the HMG-CoA reductase inhibitor fluvastatin inhibits TGF-beta1 induced TSP-1 expression via inhibition of p38 mitogen activated protein kinase (MAPK) phosphorylation in human coronary artery smooth muscle cells (HCASMC) and may therefore have anti-restenosis potential. Fluvastatin 73-84 mitogen-activated protein kinase 14 Homo sapiens 147-183 16624629-3 2006 Fluvastatin significantly reduced TSP-1 mRNA and protein expression in HCASMC in a concentration-dependent manner with a significant reduction in expression observed after treatment with 0.25 microM fluvastatin. Fluvastatin 0-11 thrombospondin 1 Homo sapiens 34-39 16624629-3 2006 Fluvastatin significantly reduced TSP-1 mRNA and protein expression in HCASMC in a concentration-dependent manner with a significant reduction in expression observed after treatment with 0.25 microM fluvastatin. Fluvastatin 199-210 thrombospondin 1 Homo sapiens 34-39 16624629-5 2006 Fluvastatin abolished TGF-beta1-induced phosphorylation of p38 MAPK and TGF-beta1-induced TSP-1 expression. Fluvastatin 0-11 transforming growth factor beta 1 Homo sapiens 22-31 16624629-5 2006 Fluvastatin abolished TGF-beta1-induced phosphorylation of p38 MAPK and TGF-beta1-induced TSP-1 expression. Fluvastatin 0-11 transforming growth factor beta 1 Homo sapiens 72-81 16624629-5 2006 Fluvastatin abolished TGF-beta1-induced phosphorylation of p38 MAPK and TGF-beta1-induced TSP-1 expression. Fluvastatin 0-11 thrombospondin 1 Homo sapiens 90-95 16624629-7 2006 We conclude that fluvastatin decreases expression of TSP-1 and abolishes the ability of TGF-beta1 to induce TSP-1 expression in HCASMC; this may be achieved by preventing signalling through the p38 MAPK pathway. Fluvastatin 17-28 thrombospondin 1 Homo sapiens 53-58 16624629-7 2006 We conclude that fluvastatin decreases expression of TSP-1 and abolishes the ability of TGF-beta1 to induce TSP-1 expression in HCASMC; this may be achieved by preventing signalling through the p38 MAPK pathway. Fluvastatin 17-28 transforming growth factor beta 1 Homo sapiens 88-97 16624629-7 2006 We conclude that fluvastatin decreases expression of TSP-1 and abolishes the ability of TGF-beta1 to induce TSP-1 expression in HCASMC; this may be achieved by preventing signalling through the p38 MAPK pathway. Fluvastatin 17-28 thrombospondin 1 Homo sapiens 108-113 16649978-0 2006 The effect of fluvastatin on plasma adiponectin levels in dyslipidaemia. Fluvastatin 14-25 adiponectin, C1Q and collagen domain containing Homo sapiens 36-47 16874687-14 2006 Fluvastatin significantly decreases Akt phosphorylation and activity in a dose-dependent manner. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 36-39 16874687-17 2006 Fluvastatin may inhibit the activity of PI3K/Akt and prevent injury to TECs from oxLDL. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 45-48 16572113-2 2006 The purpose of this study was to determine the levels of apoA-I- and apoB-containing lipoprotein subclasses before and after fluvastatin treatment of patients with chronic renal insufficiency. Fluvastatin 125-136 apolipoprotein A1 Homo sapiens 57-63 16581329-5 2006 Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). Fluvastatin 205-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 121-140 16581329-5 2006 Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). Fluvastatin 205-216 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 142-148 16630152-10 2006 RESULTS: Fluvastatin inhibited the proliferation of PBMCs and decreased the production of IL-5, IFN-gamma, CCL17, and CXCL10 after allergen-specific and non-allergen-specific stimulation; all these effects, except for decreased CXCL10 production, were partially reversed by mevalonic acid. Fluvastatin 9-20 interleukin 5 Homo sapiens 90-94 16630152-10 2006 RESULTS: Fluvastatin inhibited the proliferation of PBMCs and decreased the production of IL-5, IFN-gamma, CCL17, and CXCL10 after allergen-specific and non-allergen-specific stimulation; all these effects, except for decreased CXCL10 production, were partially reversed by mevalonic acid. Fluvastatin 9-20 interferon gamma Homo sapiens 96-105 16630152-10 2006 RESULTS: Fluvastatin inhibited the proliferation of PBMCs and decreased the production of IL-5, IFN-gamma, CCL17, and CXCL10 after allergen-specific and non-allergen-specific stimulation; all these effects, except for decreased CXCL10 production, were partially reversed by mevalonic acid. Fluvastatin 9-20 C-C motif chemokine ligand 17 Homo sapiens 107-112 16630152-10 2006 RESULTS: Fluvastatin inhibited the proliferation of PBMCs and decreased the production of IL-5, IFN-gamma, CCL17, and CXCL10 after allergen-specific and non-allergen-specific stimulation; all these effects, except for decreased CXCL10 production, were partially reversed by mevalonic acid. Fluvastatin 9-20 C-X-C motif chemokine ligand 10 Homo sapiens 118-124 16630152-10 2006 RESULTS: Fluvastatin inhibited the proliferation of PBMCs and decreased the production of IL-5, IFN-gamma, CCL17, and CXCL10 after allergen-specific and non-allergen-specific stimulation; all these effects, except for decreased CXCL10 production, were partially reversed by mevalonic acid. Fluvastatin 9-20 C-X-C motif chemokine ligand 10 Homo sapiens 228-234 16630152-11 2006 Culture supernatants obtained in the presence of fluvastatin prevented the migration of Th1 and Th2 cell lines in a dose-dependent manner. Fluvastatin 49-60 negative elongation factor complex member C/D Homo sapiens 88-91 16002074-0 2006 The association of common SNPs and haplotypes in the CETP and MDR1 genes with lipids response to fluvastatin in familial hypercholesterolemia. Fluvastatin 97-108 cholesteryl ester transfer protein Homo sapiens 53-57 16601284-11 2006 Moreover, additive anti-neoplastic effects were observed when NVP-AEW541 was combined with cytostatics such as doxorubicin or the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, fluvastatin. Fluvastatin 189-200 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 130-177 16002074-0 2006 The association of common SNPs and haplotypes in the CETP and MDR1 genes with lipids response to fluvastatin in familial hypercholesterolemia. Fluvastatin 97-108 ATP binding cassette subfamily B member 1 Homo sapiens 62-66 16002074-1 2006 OBJECTIVE: To examine whether genetic polymorphisms in the cholesteryl-ester transfer protein (CETP) and the P-glycoprotein drug transporter (MDR1), are associated with variable lipid response to fluvastatin. Fluvastatin 196-207 cholesteryl ester transfer protein Homo sapiens 59-93 16002074-1 2006 OBJECTIVE: To examine whether genetic polymorphisms in the cholesteryl-ester transfer protein (CETP) and the P-glycoprotein drug transporter (MDR1), are associated with variable lipid response to fluvastatin. Fluvastatin 196-207 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 16002074-9 2006 CONCLUSIONS: CETP and MDR1 have independent effects on lipid changes following fluvastatin treatment. Fluvastatin 79-90 cholesteryl ester transfer protein Homo sapiens 13-17 16002074-9 2006 CONCLUSIONS: CETP and MDR1 have independent effects on lipid changes following fluvastatin treatment. Fluvastatin 79-90 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 17546512-7 2006 Both Ang II-induced superoxide anion and LTC(4) generation were decreased in control cells by pertussis toxin and fluvastatin (Flu), whereas in each patient group, mepacrin, verapamil and Flu were effective, suggesting alterations in signal pathways, which may be attributed to isoprenylation. Fluvastatin 114-125 angiotensinogen Homo sapiens 5-11 16452496-7 2006 Reduction of nephrin expression by PAN and its reversal by fluvastatin were confirmed by quantitative analyses. Fluvastatin 59-70 NPHS1 adhesion molecule, nephrin Rattus norvegicus 13-20 16452496-10 2006 In addition, expression of activated membrane-bound small GTPase RhoA was markedly increased in the glomeruli of PAN nephrosis, which was inhibited by fluvastatin treatment. Fluvastatin 151-162 ras homolog family member A Rattus norvegicus 65-69 16452496-11 2006 In cultured podocytes, fluvastatin suppressed PAN-evoked activation of RhoA and actin cytoskeletal reorganization. Fluvastatin 23-34 ras homolog family member A Rattus norvegicus 71-75 16452496-14 2006 The beneficial effects of fluvastatin on podocytes can be attributable to direct modulation of excessive RhoA activity. Fluvastatin 26-37 ras homolog family member A Rattus norvegicus 105-109 16388406-5 2006 RESULTS: The acid forms had minimal inhibitory effects on all CYP activities tested, except for fluvastatin on CYP2C9-mediated tolbutamide 4-hydroxylation (IC50 = 1.7 microM) and simvastatin on CYP3A4/5-mediated paclitaxel 3-hydroxylation (12.0 microM). Fluvastatin 96-107 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 111-117 16182316-0 2006 C-reactive protein-induced upregulation of extracellular matrix metalloproteinase inducer in macrophages: inhibitory effect of fluvastatin. Fluvastatin 127-138 C-reactive protein Homo sapiens 0-18 16182316-8 2006 Fluvastatin blocked the CRP-induced increases in EMMPRIN and MMP-9 expression and activity. Fluvastatin 0-11 C-reactive protein Homo sapiens 24-27 16394514-3 2006 Although amlodipine, a calcium channel blocker, and fluvastatin, a 3-hydroxy-3-methylglutaryl CoA reductase inhibitor, show antioxidant and atheroprotective effects, the relation of AGEs to their effects is unknown. Fluvastatin 52-63 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 67-107 16317111-5 2006 In addition, fluvastatin increased IL-1beta-induced p65 nuclear translocation and nuclear factor kappaB (NF-kappaB) activity, although it inhibited those induced by LPS. Fluvastatin 13-24 interleukin 1 beta Homo sapiens 35-43 16317111-5 2006 In addition, fluvastatin increased IL-1beta-induced p65 nuclear translocation and nuclear factor kappaB (NF-kappaB) activity, although it inhibited those induced by LPS. Fluvastatin 13-24 RELA proto-oncogene, NF-kB subunit Homo sapiens 52-55 16317111-5 2006 In addition, fluvastatin increased IL-1beta-induced p65 nuclear translocation and nuclear factor kappaB (NF-kappaB) activity, although it inhibited those induced by LPS. Fluvastatin 13-24 nuclear factor kappa B subunit 1 Homo sapiens 105-114 16447234-9 2006 Apoptosis induced by fluvastatin was mitochondrial- and caspase 3-dependent and was abrogated by mevalonate and geranylgeranyl pyrophosphate, but not by farnesyl pyrophosphate. Fluvastatin 21-32 caspase 3 Homo sapiens 56-65 16447234-10 2006 In addition, the geranylgeranyl transferase inhibitor GGTI-298 mimicked the effect of fluvastatin on RA synoviocytes. Fluvastatin 86-97 protein geranylgeranyltransferase type I subunit beta Homo sapiens 54-58 16447234-12 2006 Fluvastatin decreased the amount of RhoA protein in the membrane fraction, but increased the amount in the cytosolic fraction. Fluvastatin 0-11 ras homolog family member A Homo sapiens 36-40 16447234-13 2006 CONCLUSION: Fluvastatin induced apoptosis in RA synoviocytes through a mitochondrial- and caspase 3-dependent pathway and by the blockage of mevalonate pathways, particularly through the inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathways. Fluvastatin 12-23 caspase 3 Homo sapiens 90-99 16447234-13 2006 CONCLUSION: Fluvastatin induced apoptosis in RA synoviocytes through a mitochondrial- and caspase 3-dependent pathway and by the blockage of mevalonate pathways, particularly through the inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathways. Fluvastatin 12-23 ras homolog family member A Homo sapiens 233-237 16447234-13 2006 CONCLUSION: Fluvastatin induced apoptosis in RA synoviocytes through a mitochondrial- and caspase 3-dependent pathway and by the blockage of mevalonate pathways, particularly through the inhibition of protein geranylgeranylation and RhoA/RhoA kinase pathways. Fluvastatin 12-23 ras homolog family member A Homo sapiens 238-242 16182316-8 2006 Fluvastatin blocked the CRP-induced increases in EMMPRIN and MMP-9 expression and activity. Fluvastatin 0-11 basigin (Ok blood group) Homo sapiens 49-56 16182316-8 2006 Fluvastatin blocked the CRP-induced increases in EMMPRIN and MMP-9 expression and activity. Fluvastatin 0-11 matrix metallopeptidase 9 Homo sapiens 61-66 16182316-10 2006 Fluvastatin suppressed the CRP-induced increases in 8-epi-prostaglandin F(2alpha) levels in the condition media. Fluvastatin 0-11 C-reactive protein Homo sapiens 27-30 16214041-4 2006 In this study, we showed that lovastatin, fluvastatin, atorvastatin, simvastatin, mevastatin and pravastatin are able to upregulate the mRNA expression of HO-1 gene. Fluvastatin 42-53 heme oxygenase 1 Mus musculus 155-159 17147462-22 2006 In addition, GIF data seem to reveal that fluvastatin is more likely to cause hepatic reactions than the other statins. Fluvastatin 42-53 cobalamin binding intrinsic factor Homo sapiens 13-16 17546512-7 2006 Both Ang II-induced superoxide anion and LTC(4) generation were decreased in control cells by pertussis toxin and fluvastatin (Flu), whereas in each patient group, mepacrin, verapamil and Flu were effective, suggesting alterations in signal pathways, which may be attributed to isoprenylation. Fluvastatin 127-130 angiotensinogen Homo sapiens 5-11 17546512-7 2006 Both Ang II-induced superoxide anion and LTC(4) generation were decreased in control cells by pertussis toxin and fluvastatin (Flu), whereas in each patient group, mepacrin, verapamil and Flu were effective, suggesting alterations in signal pathways, which may be attributed to isoprenylation. Fluvastatin 188-191 angiotensinogen Homo sapiens 5-11 16575466-4 2006 Water-soluble fluvastatin was used at concentrations (0-800 ng/ml) against human umbilical vein endothelial cells (HUVEC), and several well-characterized cancer cell lines in culture, including: carcinoma (LLC), melanoma (B16F1) and fibrosarcoma driven by mutant H-ras (528ras1). Fluvastatin 14-25 HRas proto-oncogene, GTPase Homo sapiens 263-268 16446645-14 2005 Our case concerns intake of fluvastatin, an HMG-CoA reductase inhibitor with rare though well-known muscular side effects: elevated serum CPK, myalgia and rhabdomyolysis. Fluvastatin 28-39 phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 alpha Homo sapiens 138-141 16166567-5 2005 Furthermore, in a whole-mount immunostaining the hypoxia-induced eNOS protein condensation with caveolin-1 of pulmonary endothelial cells was restored by the fluvastatin-treatment. Fluvastatin 158-169 nitric oxide synthase 3 Rattus norvegicus 65-69 16226226-9 2005 Combining cetuximab with TKIs (erlotinib or AG1024) or the HMG-CoA-reductase inhibitor fluvastatin or doxorubicin resulted in synergistic antiproliferative effects. Fluvastatin 87-98 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-76 16226226-10 2005 In contrast, p53 mutated Huh-7 hepatocellular cancer cells proved to be less sensitive towards cetuximab, but when combined with TKIs or fluvastatin or doxorubicin a pronounced reduction of cell growth was observed. Fluvastatin 137-148 tumor protein p53 Homo sapiens 13-16 16226226-10 2005 In contrast, p53 mutated Huh-7 hepatocellular cancer cells proved to be less sensitive towards cetuximab, but when combined with TKIs or fluvastatin or doxorubicin a pronounced reduction of cell growth was observed. Fluvastatin 137-148 MIR7-3 host gene Homo sapiens 25-30 16510370-6 2005 HDL increases (P<.01) and sdLDL decreases (P<.01) were significantly greater after fluvastatin compared with simvastatin therapy; LDL, triglycerides, ApoB, and idLDL changes were similar after both therapies (P=NS), and lbLDL decreases were greater with simvastatin therapy (P<.05). Fluvastatin 89-100 apolipoprotein B Homo sapiens 156-160 16510377-0 2005 Effects of fluvastatin treatment on lipid profile, C-reactive protein trend, and renal function in dyslipidemic patients with chronic renal failure. Fluvastatin 11-22 C-reactive protein Homo sapiens 51-69 16510377-6 2005 A statistically significant reduction in C-reactive protein (CRP) over baseline values was observed in approximately 75% of patients treated with fluvastatin. Fluvastatin 146-157 C-reactive protein Homo sapiens 41-59 16510377-6 2005 A statistically significant reduction in C-reactive protein (CRP) over baseline values was observed in approximately 75% of patients treated with fluvastatin. Fluvastatin 146-157 C-reactive protein Homo sapiens 61-64 16510377-7 2005 Furthermore, mean values of CRP for the fluvastatin standard treatment groups, respectively, were 6.78 and 10.19 at 3 months and 4.47 and 11 at 6 months. Fluvastatin 40-51 C-reactive protein Homo sapiens 28-31 16166567-5 2005 Furthermore, in a whole-mount immunostaining the hypoxia-induced eNOS protein condensation with caveolin-1 of pulmonary endothelial cells was restored by the fluvastatin-treatment. Fluvastatin 158-169 caveolin 1 Rattus norvegicus 96-106 16166567-6 2005 CONCLUSIONS: These results suggest that the fluvastatin exerts beneficial effects on chronic hypoxia-induced pulmonary hypertension by protecting against the eNOS activity at the post-transcriptional level. Fluvastatin 44-55 nitric oxide synthase 3 Rattus norvegicus 158-162 16895688-7 2005 Furthermore, fluvastatin potentiates the MHC class I upregulation but prevents MHC class II induction triggered by IFNgamma. Fluvastatin 13-24 interferon gamma Homo sapiens 115-123 16255856-1 2005 OBJECTIVE: The present study was designed to investigate the preventive and therapeutic effect of 3-hydroxy-3-methylglutanyl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on the development of atherosclerosis (AS) in immature rabbits and its possible mechanism by detecting the expression level of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the abdominal aorta. Fluvastatin 166-177 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 98-155 16255856-1 2005 OBJECTIVE: The present study was designed to investigate the preventive and therapeutic effect of 3-hydroxy-3-methylglutanyl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on the development of atherosclerosis (AS) in immature rabbits and its possible mechanism by detecting the expression level of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in the abdominal aorta. Fluvastatin 166-177 oxidized low-density lipoprotein receptor 1 Oryctolagus cuniculus 362-367 16255856-12 2005 Treatment with fluvastatin at a dosage of 10 mg/(kg.d) deduced serum lipid, attenuated artery intimal proliferation and markedly decreased the enhanced LOX-1 expression level in endothelium and neointima in immature rabbits. Fluvastatin 15-26 oxidized low-density lipoprotein receptor 1 Oryctolagus cuniculus 152-157 16255856-14 2005 CONCLUSIONS: These findings suggested that early treatment with fluvastatin not only induced a significant regression of arterial lesions of HC and early AS in immature rabbits, but also had a crucial endothelial protective effect by down-regulating LOX-1 expression level in atherosclerotic arteries in early AS. Fluvastatin 64-75 oxidized low-density lipoprotein receptor 1 Oryctolagus cuniculus 250-255 16125525-0 2005 Angiotensin II-induced oxidative burst is fluvastatin sensitive in neutrophils of patients with hypercholesterolemia. Fluvastatin 42-53 angiotensinogen Homo sapiens 0-14 16250265-0 2005 Effects of fluvastatin, an HMG-CoA reductase inhibitor, on serum levels of interleukin-18 and matrix metalloproteinase-9 in patients with hypercholesterolemia. Fluvastatin 11-22 interleukin 18 Homo sapiens 75-89 16250265-0 2005 Effects of fluvastatin, an HMG-CoA reductase inhibitor, on serum levels of interleukin-18 and matrix metalloproteinase-9 in patients with hypercholesterolemia. Fluvastatin 11-22 matrix metallopeptidase 9 Homo sapiens 94-120 16250265-4 2005 METHODS: We investigated the effects of a 12-week therapy with fluvastatin on IL-18, MMP-9, and endothelial function in patients with hypercholesterolemia. Fluvastatin 63-74 interleukin 18 Homo sapiens 78-83 16250265-4 2005 METHODS: We investigated the effects of a 12-week therapy with fluvastatin on IL-18, MMP-9, and endothelial function in patients with hypercholesterolemia. Fluvastatin 63-74 matrix metallopeptidase 9 Homo sapiens 85-90 16250265-7 2005 CONCLUSIONS: Fluvastatin reduced plasma concentrations of IL-18 and MMP-9, and improved endothelial function in patients with hypercholesterolemia independent of its lipid-lowering effect. Fluvastatin 13-24 interleukin 18 Homo sapiens 58-63 16250265-7 2005 CONCLUSIONS: Fluvastatin reduced plasma concentrations of IL-18 and MMP-9, and improved endothelial function in patients with hypercholesterolemia independent of its lipid-lowering effect. Fluvastatin 13-24 matrix metallopeptidase 9 Homo sapiens 68-73 16245407-8 2005 Reverse transcription-polymerase chain reaction and Western blot analysis showed that Cx40 and Cx43 mRNA and protein expression was elevated after injury (P < .001 for both proteins and both assays), and these elevations were suppressed by lovastatin and fluvastatin to a similar degree (P < .05 for both drugs and both assays). Fluvastatin 258-269 gap junction alpha-1 protein Oryctolagus cuniculus 95-99 16245407-12 2005 Lovastatin and fluvastatin suppress upregulated Cx40 and Cx43 expression and reduce neointimal proliferation, suggesting that Cx40 and Cx43 may play a role in statin-induced antiproliferative effect. Fluvastatin 15-26 gap junction alpha-1 protein Oryctolagus cuniculus 57-61 16245407-12 2005 Lovastatin and fluvastatin suppress upregulated Cx40 and Cx43 expression and reduce neointimal proliferation, suggesting that Cx40 and Cx43 may play a role in statin-induced antiproliferative effect. Fluvastatin 15-26 gap junction alpha-1 protein Oryctolagus cuniculus 135-139 16125525-5 2005 To sum it up, Flu administration had a beneficial effect on AII-triggered reactive oxygen species generation; it resulted in partial restoration of signaling processes and of membrane composition, but membrane fluidity remained unchanged. Fluvastatin 14-17 angiotensinogen Homo sapiens 60-63 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 117-128 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-106 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 117-128 angiotensinogen Homo sapiens 138-152 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 117-128 angiotensinogen Homo sapiens 154-157 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 130-133 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-106 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 130-133 angiotensinogen Homo sapiens 138-152 16125525-1 2005 The aim of this study was to investigate the effect of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor fluvastatin (Flu) on angiotensin II (AII)-stimulated neutrophils of patients with hypercholesterolemia. Fluvastatin 130-133 angiotensinogen Homo sapiens 154-157 16125525-2 2005 Results suggest that a 6-week-long Flu administration completely counteracted the AII-induced increase in superoxide anion and leukotriene C4 production of the neutrophils of patients with hypercholesterolemia. Fluvastatin 35-38 angiotensinogen Homo sapiens 82-85 15879517-1 2005 We investigated the effect of fluvastatin (Flv), an HMG-CoA reductase inhibitor, on Na(+)/Ca(2+) exchanger 1 (NCX1) expression in H9c2 cardiomyoblasts. Fluvastatin 30-41 solute carrier family 8 member A1 Rattus norvegicus 84-108 15901796-8 2005 Several statins inhibited the hBSEP- and rBsep-mediated uptake of TCA; however, the specific uptake of other statins (cerivastatin, fluvastatin, and pitavastatin) by hBSEP and rBSEP was not detected. Fluvastatin 132-143 ATP binding cassette subfamily B member 11 Homo sapiens 166-171 16052215-2 2005 The present study demonstrates that fluvastatin inhibits proliferation, induces apoptosis in pancreatic cancer cells harbouring a p21ras mutation at codon 12 and synergistically potentiates the cytotoxic effect of gemcitabine. Fluvastatin 36-47 HRas proto-oncogene, GTPase Homo sapiens 130-136 16052215-3 2005 The pharmacologic activities of fluvastatin are prevented by administration of mevalonic acid, suggesting that the shown inhibition of geranyl-geranylation and farnesylation of cellular proteins, including p21rhoA and p21ras, plays a major role in its anticancer effect. Fluvastatin 32-43 HRas proto-oncogene, GTPase Homo sapiens 218-224 16052215-5 2005 Moreover, fluvastatin administration significantly increases the expression of the deoxycytidine kinase, the enzyme required for the activation of gemcitabine, and simultaneously reduces the 5"-nucleotidase, responsible for deactivation of gemcitabine, suggesting a possible additional role of these enzymes in the enhanced cytotoxic activity of gemcitabine. Fluvastatin 10-21 deoxycytidine kinase Homo sapiens 83-103 16052215-5 2005 Moreover, fluvastatin administration significantly increases the expression of the deoxycytidine kinase, the enzyme required for the activation of gemcitabine, and simultaneously reduces the 5"-nucleotidase, responsible for deactivation of gemcitabine, suggesting a possible additional role of these enzymes in the enhanced cytotoxic activity of gemcitabine. Fluvastatin 10-21 5'-nucleotidase ecto Homo sapiens 191-206 16052215-7 2005 In conclusion, the combination of fluvastatin and gemcitabine is an effective cytotoxic, proapoptotic treatment in vitro and in vivo against MIAPaCa-2 cells by a mechanism of action mediated, at least in part, by the inhibition of p21ras and rhoA prenylation. Fluvastatin 34-45 HRas proto-oncogene, GTPase Homo sapiens 231-237 16052215-7 2005 In conclusion, the combination of fluvastatin and gemcitabine is an effective cytotoxic, proapoptotic treatment in vitro and in vivo against MIAPaCa-2 cells by a mechanism of action mediated, at least in part, by the inhibition of p21ras and rhoA prenylation. Fluvastatin 34-45 ras homolog family member A Homo sapiens 242-246 16029222-1 2005 We have investigated the effects of the statins atorvastatin and fluvastatin on the cytochrome P450 3A4 enzyme (CYP 3A4)-mediated metabolism of midazolam in vitro, using pooled human liver microsomes. Fluvastatin 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 84-110 16029222-1 2005 We have investigated the effects of the statins atorvastatin and fluvastatin on the cytochrome P450 3A4 enzyme (CYP 3A4)-mediated metabolism of midazolam in vitro, using pooled human liver microsomes. Fluvastatin 65-76 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 112-119 16029222-4 2005 Fluvastatin was a weak non-competitive inhibitor of CYP 3A4 with a K(i) of 94.3 (95% CI 55.01-133.5) micromol.l(-1). Fluvastatin 0-11 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 52-59 16029222-5 2005 Both atorvastatin and fluvastatin inhibit the CYP 3A4-mediated metabolism of midazolam in vitro. Fluvastatin 22-33 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 46-53 15998357-3 2005 Simvastatin, lovastatin, atorvastatin and fluvastatin were the most potent inhibitors of CYP2C8 activity with K(i) (IC(50)) values of 7.1 (9.6) muM, 8.4 (15) microM, 16 (38) microM and 19 (37) microM, respectively. Fluvastatin 42-53 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 89-95 15879517-1 2005 We investigated the effect of fluvastatin (Flv), an HMG-CoA reductase inhibitor, on Na(+)/Ca(2+) exchanger 1 (NCX1) expression in H9c2 cardiomyoblasts. Fluvastatin 30-41 solute carrier family 8 member A1 Rattus norvegicus 110-114 15879517-1 2005 We investigated the effect of fluvastatin (Flv), an HMG-CoA reductase inhibitor, on Na(+)/Ca(2+) exchanger 1 (NCX1) expression in H9c2 cardiomyoblasts. Fluvastatin 43-46 solute carrier family 8 member A1 Rattus norvegicus 84-108 15879517-1 2005 We investigated the effect of fluvastatin (Flv), an HMG-CoA reductase inhibitor, on Na(+)/Ca(2+) exchanger 1 (NCX1) expression in H9c2 cardiomyoblasts. Fluvastatin 43-46 solute carrier family 8 member A1 Rattus norvegicus 110-114 15879517-4 2005 Flv-induced down-regulation of NCX1 mRNA was also cancelled by farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP), suggesting an involvement of small G-proteins. Fluvastatin 0-3 solute carrier family 8 member A1 Rattus norvegicus 31-35 15963098-8 2005 Patients already using CYP3A4 inhibitors more frequently received fluvastatin (OR = 1.80; 95% CI 1.11, 2.94), metabolized by non-CYP3A4 pathways, and atorvastatin (OR = 1.62; 95% CI 1.06, 2.47), which is metabolized by CYP3A4, than simvastatin. Fluvastatin 66-77 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 23-29 16018822-12 2005 The stimulation of TF expression by sirolimus (20 ng/ml) was prevented by the HMG-CoA reductase inhibitor fluvastatin (1 micromol/L). Fluvastatin 106-117 coagulation factor III, tissue factor Homo sapiens 19-21 16018822-15 2005 The inhibition of TF expression by fluvastatin favors clinical use of statins in patients undergoing coronary stenting. Fluvastatin 35-46 coagulation factor III, tissue factor Homo sapiens 18-20 16226733-5 2005 Activities of caspases-8, -9, and -3 were increased in resting CD4+ T cells treated with fluvastatin (10 microM). Fluvastatin 89-100 CD4 molecule Homo sapiens 63-66 16602632-7 2005 Moreover, a relative decrease of activated MHC class I-restricted cytotoxic CD8+ T-cells was only observed upon fluvastatin treatment. Fluvastatin 112-123 CD8a molecule Homo sapiens 76-79 15802384-5 2005 Among them, HMG-CoA reductase inhibitors (cerivastatin, simvastatin, fluvastatin, and atorvastatin) enhanced the hCAR-mediated transcriptional activation of phenobarbital-responsive enhancer module reporter gene by up to 3-fold. Fluvastatin 69-80 CXADR Ig-like cell adhesion molecule Homo sapiens 113-117 15802384-9 2005 Cerivastatin, simvastatin, fluvastatin, and atorvastatin induced CYP2B6 mRNA in stable hCAR-expressed FLC7 cells but not in original FLC7 cells. Fluvastatin 27-38 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 65-71 15802384-9 2005 Cerivastatin, simvastatin, fluvastatin, and atorvastatin induced CYP2B6 mRNA in stable hCAR-expressed FLC7 cells but not in original FLC7 cells. Fluvastatin 27-38 CXADR Ig-like cell adhesion molecule Homo sapiens 87-91 16226733-0 2005 Effect of fluvastatin on apoptosis in human CD4+ T cells. Fluvastatin 10-21 CD4 molecule Homo sapiens 44-47 16226733-2 2005 We investigated the apoptotic effects of fluvastatin on peripheral CD4+ T cells from healthy subjects. Fluvastatin 41-52 CD4 molecule Homo sapiens 67-70 16226733-3 2005 Fluvastatin induced apoptosis in resting CD4+ T cells but not in CD4+ T cells strongly activated with a high concentration of PMA plus ionomycin (PMA/I) analyzed with annexin V and propidium iodide staining. Fluvastatin 0-11 CD4 molecule Homo sapiens 41-44 16226733-3 2005 Fluvastatin induced apoptosis in resting CD4+ T cells but not in CD4+ T cells strongly activated with a high concentration of PMA plus ionomycin (PMA/I) analyzed with annexin V and propidium iodide staining. Fluvastatin 0-11 annexin A5 Homo sapiens 167-176 16226733-6 2005 In strongly activated CD4+ T cells, fluvastatin inhibited the activation of caspase-8 induced by PMA/I and increased caspase-9 activity. Fluvastatin 36-47 CD4 molecule Homo sapiens 22-25 16226733-4 2005 However, CD4+ T cells activated with a low concentration of PMA/I or with anti-CD3 antibodies were apoptotic after treatment with fluvastatin. Fluvastatin 130-141 CD4 molecule Homo sapiens 9-12 16226733-5 2005 Activities of caspases-8, -9, and -3 were increased in resting CD4+ T cells treated with fluvastatin (10 microM). Fluvastatin 89-100 caspase 8 Homo sapiens 14-36 16226733-6 2005 In strongly activated CD4+ T cells, fluvastatin inhibited the activation of caspase-8 induced by PMA/I and increased caspase-9 activity. Fluvastatin 36-47 caspase 8 Homo sapiens 76-85 16226733-6 2005 In strongly activated CD4+ T cells, fluvastatin inhibited the activation of caspase-8 induced by PMA/I and increased caspase-9 activity. Fluvastatin 36-47 caspase 9 Homo sapiens 117-126 16226733-7 2005 The caspase-3 activity did not differ between untreated and fluvastatin-treated strongly activated CD4+ T cells. Fluvastatin 60-71 CD4 molecule Homo sapiens 99-102 16226733-8 2005 Treatment with fluvastatin (10 microM) enhanced cytochrome c release and increased the Bax/Bcl-2 ratio in both resting and strongly activated CD4+ T cells. Fluvastatin 15-26 cytochrome c, somatic Homo sapiens 48-60 16226733-8 2005 Treatment with fluvastatin (10 microM) enhanced cytochrome c release and increased the Bax/Bcl-2 ratio in both resting and strongly activated CD4+ T cells. Fluvastatin 15-26 BCL2 associated X, apoptosis regulator Homo sapiens 87-90 16226733-8 2005 Treatment with fluvastatin (10 microM) enhanced cytochrome c release and increased the Bax/Bcl-2 ratio in both resting and strongly activated CD4+ T cells. Fluvastatin 15-26 BCL2 apoptosis regulator Homo sapiens 91-96 16226733-8 2005 Treatment with fluvastatin (10 microM) enhanced cytochrome c release and increased the Bax/Bcl-2 ratio in both resting and strongly activated CD4+ T cells. Fluvastatin 15-26 CD4 molecule Homo sapiens 142-145 16226733-9 2005 Although the in vitro concentration of fluvastatin used in this study is higher than in vivo, other factors may sensitize apoptotic cell death of CD4+ T cells in vivo. Fluvastatin 39-50 CD4 molecule Homo sapiens 146-149 16226733-10 2005 In conclusion, fluvastatin induces apoptosis in resting T cells but not in strongly activated T cells, a difference that might be due to the interaction between caspase-8 and caspase-9. Fluvastatin 15-26 caspase 8 Homo sapiens 161-170 16226733-10 2005 In conclusion, fluvastatin induces apoptosis in resting T cells but not in strongly activated T cells, a difference that might be due to the interaction between caspase-8 and caspase-9. Fluvastatin 15-26 caspase 9 Homo sapiens 175-184 15944608-13 2005 CONCLUSIONS: These data show that Cx43 is increased in vitro during the process of intimal hyperplasia and that fluvastatin could prevent this induction, supporting a critical role for Cx43-mediated gap-junctional communication in the human vein during the development of intimal hyperplasia. Fluvastatin 112-123 gap junction protein alpha 1 Homo sapiens 185-189 15864134-0 2005 Increase in the transcriptional activity of the endothelial nitric oxide synthase gene with fluvastatin: a relation with the -786T>C polymorphism. Fluvastatin 92-103 nitric oxide synthase 3 Homo sapiens 48-81 15818460-12 2005 Incubation with 10 microM fluvastatin reduced basal expression of both ICAM-1 and PECAM-1. Fluvastatin 26-37 intercellular adhesion molecule 1 Homo sapiens 71-77 15818460-12 2005 Incubation with 10 microM fluvastatin reduced basal expression of both ICAM-1 and PECAM-1. Fluvastatin 26-37 platelet and endothelial cell adhesion molecule 1 Homo sapiens 82-89 15818460-15 2005 Incubation with 20 microM fluvastatin similarly reduced ICAM-1 expression (FI was 2014 +/- 1595 vs. 3638 +/- 1671 for the control, p = 0.02) and PECAM-1 expression (FI was 196 +/- 109 vs. 522 +/- 78 for the control, p = 0.02). Fluvastatin 26-37 intercellular adhesion molecule 1 Homo sapiens 56-62 15818460-15 2005 Incubation with 20 microM fluvastatin similarly reduced ICAM-1 expression (FI was 2014 +/- 1595 vs. 3638 +/- 1671 for the control, p = 0.02) and PECAM-1 expression (FI was 196 +/- 109 vs. 522 +/- 78 for the control, p = 0.02). Fluvastatin 26-37 platelet and endothelial cell adhesion molecule 1 Homo sapiens 145-152 15818460-21 2005 Fluvastatin thus decreases basal expression of ICAM-1 and PECAM-1. Fluvastatin 0-11 intercellular adhesion molecule 1 Homo sapiens 47-53 15818460-21 2005 Fluvastatin thus decreases basal expression of ICAM-1 and PECAM-1. Fluvastatin 0-11 platelet and endothelial cell adhesion molecule 1 Homo sapiens 58-65 15818460-22 2005 Competitive inhibition of eNOS with L-NMMA abolishes the effect of fluvastatin on ICAM-1 and PECAM-1 expression. Fluvastatin 67-78 intercellular adhesion molecule 1 Homo sapiens 82-88 15818460-22 2005 Competitive inhibition of eNOS with L-NMMA abolishes the effect of fluvastatin on ICAM-1 and PECAM-1 expression. Fluvastatin 67-78 platelet and endothelial cell adhesion molecule 1 Homo sapiens 93-100 15869627-0 2005 More on: fluvastatin inhibits up-regulation of tissue factor expression by antiphospholipid antibodies on endothelial cells. Fluvastatin 9-20 coagulation factor III, tissue factor Homo sapiens 47-60 15818460-0 2005 Nitric oxide mediates the effect of fluvastatin on intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression on human endothelial cells. Fluvastatin 36-47 intercellular adhesion molecule 1 Homo sapiens 51-84 15818460-0 2005 Nitric oxide mediates the effect of fluvastatin on intercellular adhesion molecule-1 and platelet endothelial cell adhesion molecule-1 expression on human endothelial cells. Fluvastatin 36-47 platelet and endothelial cell adhesion molecule 1 Homo sapiens 89-134 15818460-3 2005 We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Fluvastatin 32-43 intercellular adhesion molecule 1 Homo sapiens 54-87 15818460-3 2005 We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Fluvastatin 32-43 intercellular adhesion molecule 1 Homo sapiens 89-95 15818460-3 2005 We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Fluvastatin 32-43 platelet and endothelial cell adhesion molecule 1 Homo sapiens 101-146 15818460-3 2005 We examined the hypothesis that fluvastatin decreased intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1) expression through a nitric oxide-mediated pathway. Fluvastatin 32-43 platelet and endothelial cell adhesion molecule 1 Homo sapiens 148-155 15864134-2 2005 We examined endothelial nitric oxide synthase (eNOS) mRNA levels, mRNA stability and the transcriptional activities of the eNOS gene in human umbilical vein endothelial cells treated with fluvastatin and simvastatin. Fluvastatin 188-199 nitric oxide synthase 3 Homo sapiens 12-45 15864134-2 2005 We examined endothelial nitric oxide synthase (eNOS) mRNA levels, mRNA stability and the transcriptional activities of the eNOS gene in human umbilical vein endothelial cells treated with fluvastatin and simvastatin. Fluvastatin 188-199 nitric oxide synthase 3 Homo sapiens 123-127 15864134-4 2005 Utilizing the real-time reverse transcription-polymerase chain reaction, fluvastatin significantly increased eNOS mRNA levels and mRNA stability, and decreased RPA1 mRNA levels. Fluvastatin 73-84 nitric oxide synthase 3 Homo sapiens 109-113 15864134-4 2005 Utilizing the real-time reverse transcription-polymerase chain reaction, fluvastatin significantly increased eNOS mRNA levels and mRNA stability, and decreased RPA1 mRNA levels. Fluvastatin 73-84 replication protein A1 Homo sapiens 160-164 15864134-5 2005 Luciferase reporter gene assays revealed that fluvastatin significantly increased the transcriptional activity of the eNOS gene. Fluvastatin 46-57 nitric oxide synthase 3 Homo sapiens 118-122 15864134-8 2005 Fluvastatin increased eNOS mRNA levels by enhancing both the transcriptional activity and mRNA stability. Fluvastatin 0-11 nitric oxide synthase 3 Homo sapiens 22-26 15864134-9 2005 The effect of fluvastatin on the transcriptional activity was augmented in the -786C/C genotype, probably because of a decrease in RPA1 gene expression. Fluvastatin 14-25 replication protein A1 Homo sapiens 131-135 15791046-3 2005 Thus, we hypothesized that the administration of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin, which is experimentally demonstrated to have antioxidative properties as one of its pleiotropic effects, is a useful strategy for eliminating the detrimental events induced by hyperhomocysteinemia. Fluvastatin 107-118 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 49-96 15899115-12 2005 Treatment with fluvastatin improved renal function, attenuated intimal proliferation of the renal artery and markedly decreased the enhanced LOX-1 expression in the endothelium and neointima of the renal artery in rabbits. Fluvastatin 15-26 oxidized low-density lipoprotein receptor 1 Oryctolagus cuniculus 141-146 15846457-8 2005 The antidiabetic repaglinide and HMG CoA reductase inhibitor fluvastatin were found to inhibit hPEPT1 with sub-millimolar potency (IC(50) 178 +/- 1.0 and 337 +/- 4 microM, respectively). Fluvastatin 61-72 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 33-50 15550522-4 2005 Fluvastatin restored the eNOS expression and Akt phosphorylation [eNOS expression (relative intensity): LZ, 2.3 +/- 0.4; OZ, 1.0 +/- 0.2; OZ + Flu, 1.8 +/- 0.3; Akt phosphorylation (relative intensity): LZ, 2.3 +/- 0.2; OZ, 1.0 +/- 0.3; OZ + Flu, 1.9 +/- 0.2]. Fluvastatin 0-11 AKT serine/threonine kinase 1 Rattus norvegicus 45-48 15550522-4 2005 Fluvastatin restored the eNOS expression and Akt phosphorylation [eNOS expression (relative intensity): LZ, 2.3 +/- 0.4; OZ, 1.0 +/- 0.2; OZ + Flu, 1.8 +/- 0.3; Akt phosphorylation (relative intensity): LZ, 2.3 +/- 0.2; OZ, 1.0 +/- 0.3; OZ + Flu, 1.9 +/- 0.2]. Fluvastatin 0-11 AKT serine/threonine kinase 1 Rattus norvegicus 161-164 15550522-5 2005 ANG II-induced vasoconstriction was enhanced in the aortic rings of OZ rats compared with LZ rats, and this enhanced vasoconstriction was partially normalized by fluvastatin and was abolished when the aorta of OZ rats was preincubated with the Rho kinase inhibitor Y-27632. Fluvastatin 162-173 angiotensinogen Rattus norvegicus 0-6 15550522-7 2005 These results suggested that endothelium-dependent vasorelaxation was impaired, Ca(2+) sensitization of contraction was augmented in blood vessels of OZ rats and that fluvastatin restored vascular function by activating the Akt-dependent pathway and inhibiting the Rho-dependent pathway. Fluvastatin 167-178 AKT serine/threonine kinase 1 Rattus norvegicus 224-227 15846457-8 2005 The antidiabetic repaglinide and HMG CoA reductase inhibitor fluvastatin were found to inhibit hPEPT1 with sub-millimolar potency (IC(50) 178 +/- 1.0 and 337 +/- 4 microM, respectively). Fluvastatin 61-72 solute carrier family 15 member 1 Homo sapiens 95-101 15840256-1 2005 OBJECTIVE: To investigate the effects of different doses of fluvastatin on serum levels of high-sensitive C-reactive protein (hs-CRP) and tumour necrosis factor-alpha (TNFalpha) in the early phase of acute coronary syndrome (ACS). Fluvastatin 60-71 tumor necrosis factor Homo sapiens 168-176 15790413-11 2005 The primary endpoint for the study is the influence of fluvastatin therapy on levels of inflammatory markers (CRP and interleukin-6) and on pregnancy associated plasma protein A (PAPP-A). Fluvastatin 55-66 C-reactive protein Homo sapiens 110-113 15790413-11 2005 The primary endpoint for the study is the influence of fluvastatin therapy on levels of inflammatory markers (CRP and interleukin-6) and on pregnancy associated plasma protein A (PAPP-A). Fluvastatin 55-66 interleukin 6 Homo sapiens 118-131 15618295-2 2005 Pravastatin and fluvastatin also induced the production of IL-18, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in human peripheral blood mononuclear cells (PBMC) in contrast to LFA703. Fluvastatin 16-27 interleukin 18 Homo sapiens 59-64 15618295-2 2005 Pravastatin and fluvastatin also induced the production of IL-18, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in human peripheral blood mononuclear cells (PBMC) in contrast to LFA703. Fluvastatin 16-27 tumor necrosis factor Homo sapiens 66-93 15618295-2 2005 Pravastatin and fluvastatin also induced the production of IL-18, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in human peripheral blood mononuclear cells (PBMC) in contrast to LFA703. Fluvastatin 16-27 tumor necrosis factor Homo sapiens 95-104 15618295-2 2005 Pravastatin and fluvastatin also induced the production of IL-18, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in human peripheral blood mononuclear cells (PBMC) in contrast to LFA703. Fluvastatin 16-27 interferon gamma Homo sapiens 110-126 15618295-2 2005 Pravastatin and fluvastatin also induced the production of IL-18, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in human peripheral blood mononuclear cells (PBMC) in contrast to LFA703. Fluvastatin 16-27 interferon gamma Homo sapiens 128-137 15618295-5 2005 In the absence and presence of lower concentrations (0.1 and 1 ng/ml) of IL-18, pravastatin and fluvastatin inhibited the expression of intercellular adhesion molecule (ICAM)-1 and induced the expression of CD40, whereas LFA703 had no effect. Fluvastatin 96-107 intercellular adhesion molecule 1 Homo sapiens 136-176 15618295-5 2005 In the absence and presence of lower concentrations (0.1 and 1 ng/ml) of IL-18, pravastatin and fluvastatin inhibited the expression of intercellular adhesion molecule (ICAM)-1 and induced the expression of CD40, whereas LFA703 had no effect. Fluvastatin 96-107 CD40 molecule Homo sapiens 207-211 15618295-6 2005 In the presence of higher concentrations (5, 10, and 100 ng/ml) of IL-18, pravastatin, fluvastatin, and LFA703 similarly inhibited the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha, and IFN-gamma in PBMC. Fluvastatin 87-98 interleukin 18 Homo sapiens 67-72 15618295-6 2005 In the presence of higher concentrations (5, 10, and 100 ng/ml) of IL-18, pravastatin, fluvastatin, and LFA703 similarly inhibited the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha, and IFN-gamma in PBMC. Fluvastatin 87-98 intercellular adhesion molecule 1 Homo sapiens 149-155 15618295-6 2005 In the presence of higher concentrations (5, 10, and 100 ng/ml) of IL-18, pravastatin, fluvastatin, and LFA703 similarly inhibited the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha, and IFN-gamma in PBMC. Fluvastatin 87-98 CD40 molecule Homo sapiens 160-164 15618295-6 2005 In the presence of higher concentrations (5, 10, and 100 ng/ml) of IL-18, pravastatin, fluvastatin, and LFA703 similarly inhibited the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha, and IFN-gamma in PBMC. Fluvastatin 87-98 tumor necrosis factor Homo sapiens 201-210 15618295-6 2005 In the presence of higher concentrations (5, 10, and 100 ng/ml) of IL-18, pravastatin, fluvastatin, and LFA703 similarly inhibited the expression of ICAM-1 and CD40 as well as the production of IL-12, TNF-alpha, and IFN-gamma in PBMC. Fluvastatin 87-98 interferon gamma Homo sapiens 216-225 15748273-0 2005 More on: Fluvastatin inhibits upregulation of tissue factor expression by antiphospholipid antibodies on endothelial cells. Fluvastatin 9-20 coagulation factor III, tissue factor Homo sapiens 46-59 15932660-1 2005 OBJECTIVE: To investigate the effect of fluvastatin on blood levels of c-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha) and cardiac troponin I (cTnI) in patients with unstable angina undergoing percutaneous coronary intervention (PCI). Fluvastatin 40-51 C-reactive protein Homo sapiens 71-89 15932660-1 2005 OBJECTIVE: To investigate the effect of fluvastatin on blood levels of c-reactive protein (CRP), tumor necrosis factor alpha (TNFalpha) and cardiac troponin I (cTnI) in patients with unstable angina undergoing percutaneous coronary intervention (PCI). Fluvastatin 40-51 C-reactive protein Homo sapiens 91-94 15932660-4 2005 RESULTS: The serum levels of CRP, TNFalpha and cTnI in fluvastatin group were distinctly lower than those in control group before (P < 0.01) and after the procedure (P < 0.01), respectively. Fluvastatin 55-66 C-reactive protein Homo sapiens 29-32 15932660-4 2005 RESULTS: The serum levels of CRP, TNFalpha and cTnI in fluvastatin group were distinctly lower than those in control group before (P < 0.01) and after the procedure (P < 0.01), respectively. Fluvastatin 55-66 tumor necrosis factor Homo sapiens 34-42 15932660-4 2005 RESULTS: The serum levels of CRP, TNFalpha and cTnI in fluvastatin group were distinctly lower than those in control group before (P < 0.01) and after the procedure (P < 0.01), respectively. Fluvastatin 55-66 troponin I3, cardiac type Homo sapiens 47-51 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 C-reactive protein Homo sapiens 97-100 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 tumor necrosis factor Homo sapiens 102-110 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 troponin I3, cardiac type Homo sapiens 115-119 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 C-reactive protein Homo sapiens 222-225 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 tumor necrosis factor Homo sapiens 227-235 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 troponin I3, cardiac type Homo sapiens 240-244 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 C-reactive protein Homo sapiens 222-225 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 tumor necrosis factor Homo sapiens 227-235 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 161-172 troponin I3, cardiac type Homo sapiens 240-244 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 286-297 C-reactive protein Homo sapiens 222-225 15932660-5 2005 CONCLUSION: The result suggested that PCI could lead to a detectable increase in serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could significantly decrease the serum levels of CRP, TNFalpha and cTnI in patients with coronary heart disease; Fluvastatin could also decrease the serum levels of CRP, TNFalpha and cTnI in patients with PCI. Fluvastatin 286-297 C-reactive protein Homo sapiens 222-225 15698590-0 2005 Fluvastatin inhibits the expression of tumor necrosis factor-alpha and activation of nuclear factor-kappaB in human endothelial cells stimulated by C-reactive protein. Fluvastatin 0-11 tumor necrosis factor Homo sapiens 39-66 15698590-0 2005 Fluvastatin inhibits the expression of tumor necrosis factor-alpha and activation of nuclear factor-kappaB in human endothelial cells stimulated by C-reactive protein. Fluvastatin 0-11 nuclear factor kappa B subunit 1 Homo sapiens 85-106 15698590-0 2005 Fluvastatin inhibits the expression of tumor necrosis factor-alpha and activation of nuclear factor-kappaB in human endothelial cells stimulated by C-reactive protein. Fluvastatin 0-11 C-reactive protein Homo sapiens 148-166 15698590-5 2005 We determined the effects of CRP in inducing inflammatory response and the effect of fluvastatin on CRP-dependent inflammatory activation in human cultured endothelial cells. Fluvastatin 85-96 C-reactive protein Homo sapiens 100-103 15698590-11 2005 The CRP also significantly induces the activation of NF-kappaB in endothelial cells, and those effects were apparently inhibited by 10 micromol/l of fluvastatin, but not complete. Fluvastatin 149-160 C-reactive protein Homo sapiens 4-7 15698590-11 2005 The CRP also significantly induces the activation of NF-kappaB in endothelial cells, and those effects were apparently inhibited by 10 micromol/l of fluvastatin, but not complete. Fluvastatin 149-160 nuclear factor kappa B subunit 1 Homo sapiens 53-62 15698590-12 2005 CONCLUSIONS: CRP stimulation result in induction of TNF-alpha and activation of NF-kappaB, and this effect could be significantly inhibited by fluvastatin, suggesting that CRP may play a direct role in atherogenesis by activating endothelial cells, and statins inhibit this response, which may provide an insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of statins. Fluvastatin 143-154 C-reactive protein Homo sapiens 13-16 15698590-12 2005 CONCLUSIONS: CRP stimulation result in induction of TNF-alpha and activation of NF-kappaB, and this effect could be significantly inhibited by fluvastatin, suggesting that CRP may play a direct role in atherogenesis by activating endothelial cells, and statins inhibit this response, which may provide an insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of statins. Fluvastatin 143-154 tumor necrosis factor Homo sapiens 52-61 15698590-12 2005 CONCLUSIONS: CRP stimulation result in induction of TNF-alpha and activation of NF-kappaB, and this effect could be significantly inhibited by fluvastatin, suggesting that CRP may play a direct role in atherogenesis by activating endothelial cells, and statins inhibit this response, which may provide an insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of statins. Fluvastatin 143-154 nuclear factor kappa B subunit 1 Homo sapiens 80-89 15698590-12 2005 CONCLUSIONS: CRP stimulation result in induction of TNF-alpha and activation of NF-kappaB, and this effect could be significantly inhibited by fluvastatin, suggesting that CRP may play a direct role in atherogenesis by activating endothelial cells, and statins inhibit this response, which may provide an insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of statins. Fluvastatin 143-154 C-reactive protein Homo sapiens 172-175 15618295-0 2005 Differential effect of LFA703, pravastatin, and fluvastatin on production of IL-18 and expression of ICAM-1 and CD40 in human monocytes. Fluvastatin 48-59 interleukin 18 Homo sapiens 77-82 15618295-0 2005 Differential effect of LFA703, pravastatin, and fluvastatin on production of IL-18 and expression of ICAM-1 and CD40 in human monocytes. Fluvastatin 48-59 intercellular adhesion molecule 1 Homo sapiens 101-107 15618295-0 2005 Differential effect of LFA703, pravastatin, and fluvastatin on production of IL-18 and expression of ICAM-1 and CD40 in human monocytes. Fluvastatin 48-59 CD40 molecule Homo sapiens 112-116 15618295-1 2005 A novel, proinflammatory cytokine, interleukin (IL)-18 production was detected in the medium of human monocytes treated with 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibitors, pravastatin, and fluvastatin (0.1 and 1 muM) but not with the statin-derived lymphocyte function-associated antigen-1 (LFA-1) inhibitor LFA703, which did not inhibit HMG-CoA reductase. Fluvastatin 212-223 interleukin 18 Homo sapiens 35-54 15708183-2 2005 METHODS: A total of 1063 patients with single-vessel disease and 614 patients with multivessel disease were randomized to receive fluvastatin (40 mg bid) or placebo for at least 3 years following a first successful percutaneous coronary intervention. Fluvastatin 130-141 BH3 interacting domain death agonist Homo sapiens 149-152 15840256-7 2005 (2) The serum levels of hs-CRP and TNFalpha significantly lowered after one week of therapy in the two fluvastatin treated groups (P < 0.01 in all), especially in the 80 mg fluvastatin group, while no significant difference was observed before and after treatment in the routine therapy group. Fluvastatin 103-114 tumor necrosis factor Homo sapiens 35-43 15840256-7 2005 (2) The serum levels of hs-CRP and TNFalpha significantly lowered after one week of therapy in the two fluvastatin treated groups (P < 0.01 in all), especially in the 80 mg fluvastatin group, while no significant difference was observed before and after treatment in the routine therapy group. Fluvastatin 176-187 tumor necrosis factor Homo sapiens 35-43 15840256-9 2005 CONCLUSIONS: The serum levels of inflammatory factors including CRP and TNFalpha are increased in patients with ACS and early fluvastatin intervention may decease dose-dependently the serum levels of hs-CRP and TNFalpha. Fluvastatin 126-137 tumor necrosis factor Homo sapiens 72-80 15840256-9 2005 CONCLUSIONS: The serum levels of inflammatory factors including CRP and TNFalpha are increased in patients with ACS and early fluvastatin intervention may decease dose-dependently the serum levels of hs-CRP and TNFalpha. Fluvastatin 126-137 tumor necrosis factor Homo sapiens 211-219 16696316-1 2005 The expression of serum and glucocorticoid-induced protein kinase in the renal cortex of diabetic rats was examined, and the function of signal transduction mediated by SGK1 in diabetic nephropathy and its modulatiqn by fluvastatin were also investigated. Fluvastatin 220-231 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 169-173 15711752-0 2005 Fluvastatin increases the expression of adhesion molecules, monocyte chemoattractant protein-1 and tissue factor in HUVEC stimulated by patient IgG fractions containing antiphospholipid antibodies. Fluvastatin 0-11 coagulation factor III, tissue factor Homo sapiens 99-112 15711752-9 2005 The fluvastatin effect was reversed by co-incubation with mevalonate or geranylgeranylpyrophosphate and mimicked by the geranylgeranyl transferase inhibitor GGTI-286. Fluvastatin 4-15 protein geranylgeranyltransferase type I subunit beta Homo sapiens 157-161 16394614-0 2005 Enhancement of MMP-9 activity in THP-1 cells by 7-ketocholesterol and its suppression by the HMG-CoA reductase inhibitor fluvastatin. Fluvastatin 121-132 matrix metallopeptidase 9 Homo sapiens 15-20 16394614-5 2005 When fluvastatin was added to the cells, the MMP-9 activity stimulated by 7-KCHO or cholesterol decreased significantly, accompanying a decrease in the secretion of pro-MMP-9 and TIMP-1. Fluvastatin 5-16 matrix metallopeptidase 9 Homo sapiens 45-50 16394614-5 2005 When fluvastatin was added to the cells, the MMP-9 activity stimulated by 7-KCHO or cholesterol decreased significantly, accompanying a decrease in the secretion of pro-MMP-9 and TIMP-1. Fluvastatin 5-16 matrix metallopeptidase 9 Homo sapiens 169-174 16394614-5 2005 When fluvastatin was added to the cells, the MMP-9 activity stimulated by 7-KCHO or cholesterol decreased significantly, accompanying a decrease in the secretion of pro-MMP-9 and TIMP-1. Fluvastatin 5-16 TIMP metallopeptidase inhibitor 1 Homo sapiens 179-185 16394614-6 2005 The inhibition of pro-MMP-9 secretion by fluvastatin was stronger in the cells incubated with 7-KCHO than with cholesterol. Fluvastatin 41-52 matrix metallopeptidase 9 Homo sapiens 22-27 15591221-0 2005 Fluvastatin prevents vascular hyperplasia by inhibiting phenotype modulation and proliferation through extracellular signal-regulated kinase 1 and 2 and p38 mitogen-activated protein kinase inactivation in organ-cultured artery. Fluvastatin 0-11 mitogen activated protein kinase 3 Rattus norvegicus 103-148 15591221-0 2005 Fluvastatin prevents vascular hyperplasia by inhibiting phenotype modulation and proliferation through extracellular signal-regulated kinase 1 and 2 and p38 mitogen-activated protein kinase inactivation in organ-cultured artery. Fluvastatin 0-11 mitogen activated protein kinase 14 Rattus norvegicus 153-189 15591221-13 2005 Results suggest that fluvastatin inhibits vascular smooth muscle phenotype modulation and proliferation by inhibiting the ERK1/2 and p38MAPK activities through depletion of mevalonate in smooth muscle cells, resulting in inhibiting vascular hyperplastic changes. Fluvastatin 21-32 mitogen activated protein kinase 3 Rattus norvegicus 122-128 15591221-13 2005 Results suggest that fluvastatin inhibits vascular smooth muscle phenotype modulation and proliferation by inhibiting the ERK1/2 and p38MAPK activities through depletion of mevalonate in smooth muscle cells, resulting in inhibiting vascular hyperplastic changes. Fluvastatin 21-32 mitogen activated protein kinase 14 Rattus norvegicus 133-140 15711752-0 2005 Fluvastatin increases the expression of adhesion molecules, monocyte chemoattractant protein-1 and tissue factor in HUVEC stimulated by patient IgG fractions containing antiphospholipid antibodies. Fluvastatin 0-11 C-C motif chemokine ligand 2 Homo sapiens 60-94 16696316-7 2005 The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. Fluvastatin 111-122 transforming growth factor, beta 1 Rattus norvegicus 71-80 16696316-10 2005 Fluvastatin suppressed the increased SGK1mRNA expression in renal cortex and postponed the development of diabetic nephropathy. Fluvastatin 0-11 serum/glucocorticoid regulated kinase 1 Rattus norvegicus 37-41 15389871-7 2004 However, BMP-2 is unlikely to play a positive role in neuroglial differentiation of MSCs since its expression was down-regulated in fluvastatin-treated cells. Fluvastatin 132-143 bone morphogenetic protein 2 Homo sapiens 9-14 15957541-3 2005 Major medical literature databases were searched for published information about fluvastatin, a HMG-CoA reductase inhibitor, used in patients with impaired renal function. Fluvastatin 81-92 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 96-113 15623649-0 2004 3-hydroxy-3-methylglutaryl-coenzyme a reductase inhibitor, fluvastatin, as a novel agent for prophylaxis of renal cancer metastasis. Fluvastatin 59-70 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 0-47 15581350-5 2004 Mutation of arginine 241 had marked effects on the hydroxylation of anionic substrates of CYP2C8 such as retinoic acid and fluvastatin. Fluvastatin 123-134 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 90-96 15581350-9 2004 The S114F and F205A mutants were the best catalysts for retinoic acid and paclitaxel (or fluvastatin) hydroxylation, respectively, with k(cat)/K(m) values 5 and 2.1 (or 2.4) times higher, respectively, than those found for CYP2C8. Fluvastatin 89-100 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 223-229 15537494-6 2004 Fluvastatin reduced production of Th1-type cytokines, including interferon (IFN)-gamma and interleukin (IL)-2, and inhibited expression of inflammatory cytokine mRNAs in the myocardium. Fluvastatin 0-11 interleukin 2 Rattus norvegicus 91-109 15537494-7 2004 Infiltration of CD4-positive T cells into the myocardium and T cell proliferative responses were suppressed by fluvastatin. Fluvastatin 111-122 Cd4 molecule Rattus norvegicus 16-19 15624040-0 2004 Fluvastatin reduces oxidative stress, decreases serum monocyte chemotactic protein-1 level and improves endothelial function in patients with hypercholesterolemia. Fluvastatin 0-11 C-C motif chemokine ligand 2 Homo sapiens 54-84 15624040-5 2004 RESULTS: Fluvastatin significantly reduced the serum level of total cholesterol (201.8 +/- 25.2 vs 271.6 +/- 24.7 mg/dL; p < 0.001), low-density lipoprotein cholesterol (129.4 +/- 5.1 vs 190.2 +/- 19 mg/dL; p < 0.001), MCP-1 (190.3 +/- 40 vs 217.6 +/- 61 pg/mL; p = 0.001), and TBARS (3.7 +/- 1.3 vs 5.2 +/- 1.4 nmol/mL; p < 0.001). Fluvastatin 9-20 C-C motif chemokine ligand 2 Homo sapiens 225-230 29793229-5 2004 CYP2C9 metabolizes several oral hypoglycemics, oral anticoagulants, non-steroidal anti-inflammatory drugs and other drugs, including phenytoin, losartan, fluvastatin, and torsemide. Fluvastatin 154-165 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 0-6 15569838-4 2004 The effect of thrombin was prevented by C3 exoenzyme or the HMG-CoA reductase inhibitor fluvastatin, which inhibit RhoA, or by the ROCK inhibitors Y-27632 and HA-1077. Fluvastatin 88-99 coagulation factor II, thrombin Homo sapiens 14-22 15569838-4 2004 The effect of thrombin was prevented by C3 exoenzyme or the HMG-CoA reductase inhibitor fluvastatin, which inhibit RhoA, or by the ROCK inhibitors Y-27632 and HA-1077. Fluvastatin 88-99 ras homolog family member A Homo sapiens 115-119 15530865-2 2004 In this study, we found in murine RAW264.7 macrophages, statins within 1-30 microM stimulated COX-2 gene transcription and PGE(2) formation, displaying potencies as lovastatin > fluvastatin > atorvastatin >> pravastatin. Fluvastatin 181-192 cytochrome c oxidase II, mitochondrial Mus musculus 94-99 15662091-0 2004 Effect of simvastatin and fluvastatin on plasma fibrinogen levels in patients with primary hypercholesterolemia. Fluvastatin 26-37 fibrinogen beta chain Homo sapiens 48-58 15452025-0 2004 Fluvastatin enhances the inhibitory effects of a selective AT1 receptor blocker, valsartan, on atherosclerosis. Fluvastatin 0-11 angiotensin II receptor, type 1a Mus musculus 59-62 15452025-7 2004 Similar inhibitory effects of valsartan or fluvastatin on the expressions of nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide phosphate oxidase subunits p22phox and p47phox, production of superoxide anion, the expression of monocyte chemoattractant protein-1, and intercellular adhesion molecule-1 expression were observed. Fluvastatin 43-54 cytochrome b-245, alpha polypeptide Mus musculus 172-179 15483743-7 2004 (1) Whereas no modification in CD25 expression was seen, fluvastatin at 5 microM caused a lower level of CD69 expression, accompanied by an essential suppression on proliferation, IL-2 production and cytotoxicity development in PHA-stimulated T cells. Fluvastatin 57-68 CD69 molecule Homo sapiens 105-109 15483743-7 2004 (1) Whereas no modification in CD25 expression was seen, fluvastatin at 5 microM caused a lower level of CD69 expression, accompanied by an essential suppression on proliferation, IL-2 production and cytotoxicity development in PHA-stimulated T cells. Fluvastatin 57-68 interleukin 2 Homo sapiens 180-184 15483743-9 2004 (2) Combined with cyclosporine A (CsA), fluvastatin would further repress CD69 expression, cells proliferation and activity of killer cells, meanwhile significantly induced the secretion of IL-4 and IL-10. Fluvastatin 40-51 CD69 molecule Homo sapiens 74-78 15483743-9 2004 (2) Combined with cyclosporine A (CsA), fluvastatin would further repress CD69 expression, cells proliferation and activity of killer cells, meanwhile significantly induced the secretion of IL-4 and IL-10. Fluvastatin 40-51 interleukin 4 Homo sapiens 190-194 15483743-9 2004 (2) Combined with cyclosporine A (CsA), fluvastatin would further repress CD69 expression, cells proliferation and activity of killer cells, meanwhile significantly induced the secretion of IL-4 and IL-10. Fluvastatin 40-51 interleukin 10 Homo sapiens 199-204 15598476-14 2004 The ICER showed that each 1% decrease in LDL-C level achieved with the fenofibrate + fluvastatin combination added a cost of 14.97 Euros/y (US 12.25 US dollars/y), and each 1% increase in HDL-C level added a cost of 7.48 Euros/y (6.12/y US dollars), over the cost of monotherapy. Fluvastatin 85-96 component of oligomeric golgi complex 2 Homo sapiens 41-46 15518777-15 2004 Fluvastatin significantly produced a reduction rate in TC of 16%, TG of 22%, and LDL-C of 5% after 6 months of treatment, respectively. Fluvastatin 0-11 component of oligomeric golgi complex 2 Homo sapiens 81-86 15350166-3 2004 Fluvastatin (Lescol, Novartis Pharmaceuticals) was the first totally synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor on the market and has recently become available in an extended-release formulation (Lescol XL, Novartis Pharmaceuticals). Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 79-126 15350166-6 2004 The demonstration of the safe use of fluvastatin in a wide range of patients may be associated with the predominant acid form of the drug in vivo, as well as its predominant metabolism via the cytochrome P450 2C9 pathway. Fluvastatin 37-48 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 193-212 15333031-0 2004 Fluvastatin inhibits up-regulation of tissue factor expression by antiphospholipid antibodies on endothelial cells. Fluvastatin 0-11 coagulation factor III, tissue factor Homo sapiens 38-51 15333031-10 2004 Fluvastatin (10 micro m) inhibited the effects of PMA and the four IgG-APS on TF expression by 70, 47, 65, 22 and 68%, respectively, and this effect was dose-dependent. Fluvastatin 0-11 coagulation factor III, tissue factor Homo sapiens 78-80 15333031-11 2004 Mevalonate (100 micro m) completely abrogated the inhibitory effects of fluvastatin on TF expression induced by aPL. Fluvastatin 72-83 coagulation factor III, tissue factor Homo sapiens 87-89 15518777-20 2004 CONCLUSIONS: Fluvastatin seemed to be safe and highly effective to control TC, TG, LDL-C, and HDL-C in renal transplant recipients. Fluvastatin 13-24 component of oligomeric golgi complex 2 Homo sapiens 83-88 15462110-8 2004 Fluvastatin treatment significantly lowered serum total cholesterol, low-density lipoprotein (LDL) cholesterol and apo-lipoprotein B concentrations by 16%, 25%, and 22%, respectively, compared with patients receiving dietary therapy alone. Fluvastatin 0-11 apolipoprotein B Homo sapiens 115-132 15276654-5 2004 A pull-down assay demonstrated fluvastatin to decrease levels of GTP-bound Rho A. Fluvastatin 31-42 ras homolog family member A Homo sapiens 75-80 15207698-6 2004 The addition of fluvastatin to TNF-alpha-activated HCAECs significantly suppressed EMP release. Fluvastatin 16-27 tumor necrosis factor Homo sapiens 31-40 15207698-7 2004 Fluvastatin suppressed TNF-alpha-induced Rho activation. Fluvastatin 0-11 tumor necrosis factor Homo sapiens 23-32 15207698-9 2004 CONCLUSION: EMP release from TNF-alpha-activated HCAECs is suppressed by fluvastatin. Fluvastatin 73-84 tumor necrosis factor Homo sapiens 29-38 15205386-3 2004 In the present study, in vitro enzyme kinetic data were used to predict the in vivo clearance and drug-drug interaction potential of four well known CYP2C9 substrates (tolbutamide, fluvastatin, ibuprofen and diclofenac) that are frequently used as benchmark substances in screening programs. Fluvastatin 181-192 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 149-155 15309245-8 2004 In contrast, treatment with fluvastatin (40 mg, n = 50) or ciprofibrate (100 mg, n = 40) reduced by 25% plasma PAF-AH activity (P <.001) associated with a decrease in serum levels of total cholesterol and LDL-cholesterol (P <.001). Fluvastatin 28-39 phospholipase A2 group VII Homo sapiens 111-117 15166180-7 2004 Cerivastatin, pitavastatin, and fluvastatin inhibited atherosclerotic lesion progression in apolipoprotein E-deficient mice, whereas they augmented blood flow recovery and capillary formation in ischemic hind limb. Fluvastatin 32-43 apolipoprotein E Mus musculus 92-108 15169608-7 2004 Avasimibe, fluvastatin, and PPARalpha agonists (fenofibric acid and Wy-14643) significantly reduced, in a concentration-dependent manner, MMP-9 protein (up to 67 +/- 5% for fenofibric acid). Fluvastatin 11-22 matrix metallopeptidase 9 Homo sapiens 138-143 15173604-3 2004 With the aim of enhancing the nonlipid-lowering properties of selected statins, we introduced a NO-releasing moiety into the structure of pravastatin (NCX 6550) and fluvastatin (NCX 6553). Fluvastatin 165-176 solute carrier family 8 member A1 Rattus norvegicus 178-181 15370294-5 2004 Id1 was up-regulated by fluvastatin and serum, but not by VEGF and HGF. Fluvastatin 24-35 inhibitor of DNA binding 1, HLH protein Homo sapiens 0-3 15370294-6 2004 Fluvastatin did not regulate p21 and p27, but down-regulated Id3 and p53 slightly. Fluvastatin 0-11 inhibitor of DNA binding 3, HLH protein Homo sapiens 61-64 15370294-6 2004 Fluvastatin did not regulate p21 and p27, but down-regulated Id3 and p53 slightly. Fluvastatin 0-11 tumor protein p53 Homo sapiens 69-72 14975748-7 2004 Further, fluvastatin reduced Akt phosphorylation and dominant-negative Akt inhibited PDGF-induced osteoblast migration. Fluvastatin 9-20 thymoma viral proto-oncogene 1 Mus musculus 29-32 15033469-3 2004 We tested the effects of four different statins (fluvastatin, atorvastatin, simvastatin, and lovastatin) on ABCA1 expression in macrophages in vitro. Fluvastatin 49-60 ATP binding cassette subfamily A member 1 Homo sapiens 108-113 15001601-9 2004 Fluvastatin treatment decreased the activity of PAF-AH by 22.8% compared with an increase of 0.4% in the placebo group (P < 0.001). Fluvastatin 0-11 phospholipase A2 group VII Homo sapiens 48-54 15001601-0 2004 Fluvastatin slow-release lowers platelet-activating factor acetyl hydrolase activity: a placebo-controlled trial in patients with type 2 diabetes. Fluvastatin 0-11 phospholipase A2 group VII Homo sapiens 32-75 15001601-12 2004 Fluvastatin not only decreases atherogenic dLDL but also PAF-AH activity, emphasizing the significance of fluvastatin treatment in T2DM. Fluvastatin 0-11 modular serine protease Drosophila melanogaster 43-47 15001601-1 2004 Fluvastatin reduces atherogenic dense low-density lipoprotein (dLDL) in patients with type 2 diabetes mellitus (T2DM). Fluvastatin 0-11 modular serine protease Drosophila melanogaster 63-67 15001601-12 2004 Fluvastatin not only decreases atherogenic dLDL but also PAF-AH activity, emphasizing the significance of fluvastatin treatment in T2DM. Fluvastatin 0-11 phospholipase A2 group VII Homo sapiens 57-63 15001601-13 2004 The antiatherogenic potential of fluvastatin in T2DM may thus be greater than expected from its effects on LDL-C and triglycerides alone. Fluvastatin 33-44 modular serine protease Drosophila melanogaster 107-110 15019531-7 2004 In addition, Fcgamma receptor mediated immune complex trafficking, activation of MAP kinases (ERK and p38), and downstream inflammatory mediator release (MMP-1 and IL-6) were blocked by fluvastatin. Fluvastatin 186-197 mitogen-activated protein kinase 14 Homo sapiens 102-105 15019531-7 2004 In addition, Fcgamma receptor mediated immune complex trafficking, activation of MAP kinases (ERK and p38), and downstream inflammatory mediator release (MMP-1 and IL-6) were blocked by fluvastatin. Fluvastatin 186-197 matrix metallopeptidase 1 Homo sapiens 154-159 15019531-7 2004 In addition, Fcgamma receptor mediated immune complex trafficking, activation of MAP kinases (ERK and p38), and downstream inflammatory mediator release (MMP-1 and IL-6) were blocked by fluvastatin. Fluvastatin 186-197 interleukin 6 Homo sapiens 164-168 14729100-6 2004 Fluvastatin inhibited organic anion uptake mediated by human OAT1 in a mixture of competitive and noncompetitive manner, whereas simvastatin and fluvastatin noncompetitively inhibited the organic anion uptake mediated by human OAT3. Fluvastatin 0-11 solute carrier family 22 member 6 Homo sapiens 61-65 14729100-6 2004 Fluvastatin inhibited organic anion uptake mediated by human OAT1 in a mixture of competitive and noncompetitive manner, whereas simvastatin and fluvastatin noncompetitively inhibited the organic anion uptake mediated by human OAT3. Fluvastatin 145-156 solute carrier family 22 member 8 Homo sapiens 227-231 15153664-0 2004 Effects of fluvastatin in type 2 diabetic patients with hyperlipidemia: reduction in cholesterol oxidation products and VCAM-1. Fluvastatin 11-22 vascular cell adhesion molecule 1 Homo sapiens 120-126 15153664-1 2004 The purpose of this study was to investigate the lipid-lowering and anti-oxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, in type 2 diabetic patients. Fluvastatin 94-105 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 109-166 15153664-8 2004 Finally, VCAM-1 levels were similarly reduced by fluvastatin treatment. Fluvastatin 49-60 vascular cell adhesion molecule 1 Homo sapiens 9-15 15331935-7 2004 The majority of fluvastatin-treated cells were arrested at the G1 phase, associated with down-regulation of cyclin A and up-regulation of cyclin-dependent kinase inhibitor p27kip1, indicating that cell cycle modulation is an important mechanism. Fluvastatin 16-27 cyclin-dependent kinase inhibitor 1B Rattus norvegicus 172-179 14668577-3 2004 Fluvastatin (20 mg/kg/d) reduced plasma PON1 activity toward paraoxon and phenyl acetate by 23.6% and 17.4%, respectively. Fluvastatin 0-11 paraoxonase 1 Rattus norvegicus 40-44 14668577-5 2004 PON1 activity toward paraoxon in the liver of rats treated with 20 mg/kg/d fluvastatin was 27.5% lower than in the control group, and the activity toward phenyl acetate was reduced by 25.4% and 35.9% in rats receiving 2 and 20 mg/kg/d of this drug, respectively. Fluvastatin 75-86 paraoxonase 1 Rattus norvegicus 0-4 14668577-6 2004 Fluvastatin at 2 and 20 mg/kg/d also decreased cardiac PON1 by 31.3% and 27.3%, respectively. Fluvastatin 0-11 paraoxonase 1 Rattus norvegicus 55-59 14668577-9 2004 It is concluded that fluvastatin reduces PON1 activity more efficiently than does pravastatin. Fluvastatin 21-32 paraoxonase 1 Rattus norvegicus 41-45 15331935-8 2004 Fluvastatin significantly decreased messenger RNA expression of type III collagen and connective tissue growth factor. Fluvastatin 0-11 myotrophin Rattus norvegicus 104-117 14644448-2 2003 In this study, we showed that lovastatin and fluvastatin are able to upregulate the mRNA expression of the suppressor of cytokine signaling-3 (SOCS-3) gene. Fluvastatin 45-56 suppressor of cytokine signaling 3 Homo sapiens 107-141 15128052-2 2004 Our objectives were to determine the effects of PPAR haplotypes on biochemical, angiographic, clinical phenotypes and their responses to treatment with fluvastatin. Fluvastatin 152-163 peroxisome proliferator activated receptor alpha Homo sapiens 48-52 15128052-7 2004 The baseline plasma triglyceride levels and their responses to treatment with fluvastatin were associated with PPARD haplotypes (P = 0.01). Fluvastatin 78-89 peroxisome proliferator activated receptor delta Homo sapiens 111-116 15128052-9 2004 PPARD haplotype 3 was also an independent determinant of plasma apolipoprotein (apo)B (P = 0.021) and apoC-III (P = 0.001) levels, mean number of coronary lesions (P = 0.046) and changes in triglyceride (P = 0.01) and apoC-III (P = 0.047) levels in response to fluvastatin. Fluvastatin 261-272 peroxisome proliferator activated receptor delta Homo sapiens 0-5 15507280-8 2004 Upregulation of TF on ECs can also be abrogated by treatment of the cells with fluvastatin. Fluvastatin 79-90 coagulation factor III Mus musculus 16-18 14644448-2 2003 In this study, we showed that lovastatin and fluvastatin are able to upregulate the mRNA expression of the suppressor of cytokine signaling-3 (SOCS-3) gene. Fluvastatin 45-56 suppressor of cytokine signaling 3 Homo sapiens 143-149 14629460-7 2003 RESULTS: Pretreatment with simvastatin, fluvastatin or pravastatin potentiated the TNF-alpha and LPS-induced expression of E-selectin and VCAM-1, and mevalonate reversed the potentiating effect of these statins. Fluvastatin 40-51 tumor necrosis factor Homo sapiens 83-92 14665719-0 2003 Fluvastatin improves insulin resistance in nondiabetic dyslipidemic patients. Fluvastatin 0-11 insulin Homo sapiens 21-28 14665719-8 2003 Fasting plasma triglyceride, total and LDL cholesterol, fasting insulin, and HOMA index were significantly reduced and HDL cholesterol was improved after fluvastatin treatment. Fluvastatin 154-165 insulin Homo sapiens 64-71 14665719-12 2003 As a conclusion, the present study indicates that fluvastatin treatment improves insulin resistance in dyslipidemic patients who do not have diabetes or impaired fasting glucose. Fluvastatin 50-61 insulin Homo sapiens 81-88 14665719-13 2003 Also, the effect of fluvastatin on insulin resistance is not associated with the lowering of triglycerides. Fluvastatin 20-31 insulin Homo sapiens 35-42 15259790-0 2003 Time-dependent lipid response on fluvastatin therapy of patients with hypercholesterolemia sensitive to apoE phenotype. Fluvastatin 33-44 apolipoprotein E Homo sapiens 104-108 14583185-7 2003 RESULTS: Both the increased neutrophil-endothelial cell adhesion and ICAM-1 expression caused by high insulin (100 microU/ml) for 48 h were significantly attenuated by pretreatment with cerivastatin (0.01 microM), but not by fluvastatin (0.5 microM) or pravastatin (0.05 microM). Fluvastatin 225-236 insulin Homo sapiens 102-109 14629460-7 2003 RESULTS: Pretreatment with simvastatin, fluvastatin or pravastatin potentiated the TNF-alpha and LPS-induced expression of E-selectin and VCAM-1, and mevalonate reversed the potentiating effect of these statins. Fluvastatin 40-51 selectin E Homo sapiens 123-133 14629460-7 2003 RESULTS: Pretreatment with simvastatin, fluvastatin or pravastatin potentiated the TNF-alpha and LPS-induced expression of E-selectin and VCAM-1, and mevalonate reversed the potentiating effect of these statins. Fluvastatin 40-51 vascular cell adhesion molecule 1 Homo sapiens 138-144 12967585-0 2003 HMG-CoA reductase inhibitor, fluvastatin, has cholesterol-lowering independent "direct" effects on atherosclerotic vessels in high cholesterol diet-fed rabbits. Fluvastatin 29-40 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 0-17 14521748-0 2003 [The expression of connective tissue growth factor in renal cortex of 5/6 nephrectomized rats and its modulation by fluvastatin]. Fluvastatin 116-127 cellular communication network factor 2 Rattus norvegicus 19-50 12964001-5 2003 Fluvastatin inhibited LPA-induced translocation of RhoA protein from the cytosol to the membrane and RhoA activation which was measured by pull-down assay for GTP-bound RhoA. Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 51-55 12964001-5 2003 Fluvastatin inhibited LPA-induced translocation of RhoA protein from the cytosol to the membrane and RhoA activation which was measured by pull-down assay for GTP-bound RhoA. Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 101-105 12964001-5 2003 Fluvastatin inhibited LPA-induced translocation of RhoA protein from the cytosol to the membrane and RhoA activation which was measured by pull-down assay for GTP-bound RhoA. Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 101-105 12964001-6 2003 Fluvastatin also inhibited the translocation of both endogenous and dominant-active RhoA from the cytosol to the membrane, actin stress fiber assembly and in vitro invasion of the cells expressing dominant-active RhoA (Val14-RhoA). Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 84-88 12964001-6 2003 Fluvastatin also inhibited the translocation of both endogenous and dominant-active RhoA from the cytosol to the membrane, actin stress fiber assembly and in vitro invasion of the cells expressing dominant-active RhoA (Val14-RhoA). Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 213-217 12964001-6 2003 Fluvastatin also inhibited the translocation of both endogenous and dominant-active RhoA from the cytosol to the membrane, actin stress fiber assembly and in vitro invasion of the cells expressing dominant-active RhoA (Val14-RhoA). Fluvastatin 0-11 ras homolog family member A Rattus norvegicus 219-229 14666702-0 2003 HMG CoA reductase inhibitor fluvastatin arrests the development of implanted hepatocarcinoma in rats. Fluvastatin 28-39 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 0-17 14518599-11 2003 The differences in the potency of statins (Cer > Atv > Sim > Pra > Lov > Flu) were also reflected at the transcriptional level and the protein level of NF-kappaB controlled tissue factor expression. Fluvastatin 88-91 nuclear factor kappa B subunit 1 Homo sapiens 167-176 14518599-11 2003 The differences in the potency of statins (Cer > Atv > Sim > Pra > Lov > Flu) were also reflected at the transcriptional level and the protein level of NF-kappaB controlled tissue factor expression. Fluvastatin 88-91 coagulation factor III, tissue factor Homo sapiens 188-201 14612203-4 2003 Lovastatin, simvastatin, atorvastatin, fluvastatin and cerivastatin, which are hydrophobic statins, markedly reduced cell viability associated with DNA fragmentation, DNA laddering and activation of caspase-3, suggesting apoptotic cell death. Fluvastatin 39-50 caspase 3 Rattus norvegicus 199-208 14521748-1 2003 OBJECTIVE: To investigate the connective tissue growth factor (CTGF) mRNA expression in the renal cortex of 5/6 nephrectomized rats and its modulation by fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Fluvastatin 154-165 cellular communication network factor 2 Rattus norvegicus 30-61 14521748-1 2003 OBJECTIVE: To investigate the connective tissue growth factor (CTGF) mRNA expression in the renal cortex of 5/6 nephrectomized rats and its modulation by fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Fluvastatin 154-165 cellular communication network factor 2 Rattus norvegicus 63-67 14521748-1 2003 OBJECTIVE: To investigate the connective tissue growth factor (CTGF) mRNA expression in the renal cortex of 5/6 nephrectomized rats and its modulation by fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Fluvastatin 154-165 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 169-216 14521748-17 2003 The glomerular protein expressions of TGF-beta1, type IV collagen and fibronectin were significantly weaker in the fluvastatin treatment group as compared with the model group (all P<0.01). Fluvastatin 115-126 transforming growth factor, beta 1 Rattus norvegicus 38-47 14521748-17 2003 The glomerular protein expressions of TGF-beta1, type IV collagen and fibronectin were significantly weaker in the fluvastatin treatment group as compared with the model group (all P<0.01). Fluvastatin 115-126 fibronectin 1 Rattus norvegicus 70-81 14521748-19 2003 Fluvastatin suppresses the increased CTGF mRNA expression in renal cortex and ameliorates the glomerular extracellular matrix accumulation. Fluvastatin 0-11 cellular communication network factor 2 Rattus norvegicus 37-41 12815175-8 2003 Y-27632 (1-10 microM), a specific Rho-kinase inhibitor, and fluvastatin (10 microM), an indirect inhibitor for Rho proteins, significantly inhibited the IL-1beta-induced effects on the channel activity and production of oxygen radicals. Fluvastatin 60-71 interleukin-1 beta Oryctolagus cuniculus 153-161 12623790-9 2003 Furthermore, fluvastatin induced a significant reduction of MPO activity and an increase of cGMP level compared with the control group. Fluvastatin 13-24 myeloperoxidase Rattus norvegicus 60-63 12891229-2 2003 The consequences of CYP2C9 genetic polymorphisms on fluvastatin pharmacokinetics and on its efficacy have not been investigated in humans thus far. Fluvastatin 52-63 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 20-26 12891229-19 2003 CONCLUSIONS: The pharmacokinetics of both enantiomers of fluvastatin depended on the CYP2C9 genotype, with a 3-fold group mean difference in the active enantiomer and even greater differences in the inactive enantiomer, but differences in plasma concentrations were not reflected in cholesterol lowering after 14 days of fluvastatin intake in healthy volunteers. Fluvastatin 57-68 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-91 12891229-19 2003 CONCLUSIONS: The pharmacokinetics of both enantiomers of fluvastatin depended on the CYP2C9 genotype, with a 3-fold group mean difference in the active enantiomer and even greater differences in the inactive enantiomer, but differences in plasma concentrations were not reflected in cholesterol lowering after 14 days of fluvastatin intake in healthy volunteers. Fluvastatin 321-332 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-91 12808293-1 2003 We previously reported that fluvastatin, a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, a strong lipid lowering drug, exerted an anti-atherosclerotic effect at doses insufficient to lower serum lipids in cholesterol fed rabbits. Fluvastatin 28-39 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 50-107 12852707-4 2003 With the immediate-release (IR) formulation of fluvastatin, the maximal dose of 80 mg is recommended to be administered in divided doses (40 mg BID). Fluvastatin 47-58 BH3 interacting domain death agonist Homo sapiens 144-147 12748879-7 2003 Simvastatin, atorvastatin, and fluvastatin reduced monocyte procoagulant activity in whole blood and P-selectin (P<0.01). Fluvastatin 31-42 selectin P Homo sapiens 101-111 12667961-10 2003 Fluvastatin and cerivastatin also reduced the activation of NF-kappaB by CRP. Fluvastatin 0-11 nuclear factor kappa B subunit 1 Homo sapiens 60-69 12667961-10 2003 Fluvastatin and cerivastatin also reduced the activation of NF-kappaB by CRP. Fluvastatin 0-11 C-reactive protein Homo sapiens 73-76 24944371-10 2003 RESULTS: The plasma levels of LDL cholesterol (LDL-C) and apolipoprotein (apo) B were reduced by 25% and 17%, respectively (P<0.001 for both), after 12 weeks of treatment with fluvastatin 20 mg/d; no further significant reductions in LDL were observed after increasing the daily dose to 40 mg. Fluvastatin 20 mg/d for 12 weeks decreased plasma levels of intermediate-density lipoprotein cholesterol, LDL-I-C, LDL-II-C, and LDL-III-C by 25% (P<0.01), 30% (P<0.001), 23% (P<0.01), and 20% (P = 0.02), respectively. Fluvastatin 179-190 component of oligomeric golgi complex 2 Homo sapiens 47-80 24944371-10 2003 RESULTS: The plasma levels of LDL cholesterol (LDL-C) and apolipoprotein (apo) B were reduced by 25% and 17%, respectively (P<0.001 for both), after 12 weeks of treatment with fluvastatin 20 mg/d; no further significant reductions in LDL were observed after increasing the daily dose to 40 mg. Fluvastatin 20 mg/d for 12 weeks decreased plasma levels of intermediate-density lipoprotein cholesterol, LDL-I-C, LDL-II-C, and LDL-III-C by 25% (P<0.01), 30% (P<0.001), 23% (P<0.01), and 20% (P = 0.02), respectively. Fluvastatin 297-308 component of oligomeric golgi complex 2 Homo sapiens 47-80 24944371-13 2003 However, plasma levels of Ox-LDL-IgG and soluble P-selectin did not decrease after 12 weeks of fluvastatin 20 mg/d, but did decrease significantly (both 22%) after the next 12 weeks of treatment with fluvastatin 40 mg/d (P<0.05). Fluvastatin 200-211 selectin P Homo sapiens 49-59 24944371-16 2003 CONCLUSIONS: In this patient population, fluvastatin 20 mg/d was sufficient to significantly reduce plasma levels of LDL, the 3 LDL subfractions, and Ox-LDL, but was not sufficient to reduce plasma levels of Ox-LDL-IgG and soluble P-selectin. Fluvastatin 41-52 selectin P Homo sapiens 231-241 12722044-0 2003 Effect of a 3-year therapy with the 3-hydroxy-3-methylglutaryl coenzyme a reductase-inhibitor fluvastatin on endothelial function and distensibility of large arteries in hypercholesterolemic renal transplant recipient. Fluvastatin 94-105 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 36-83 12706457-2 2003 The dose-response relationships for the above effects show that simvastatin, atorvastatin and fluvastatin affect linoleic acid conversion and the delta5 desaturase step more potently than the synthesis of cholesterol, simvastatin being the most effective in inhibiting sterol synthesis, whereas atorvastatin in stimulating the conversion of linoleic acid. Fluvastatin 94-105 fatty acid desaturase 1 Homo sapiens 146-163 12852707-16 2003 CONCLUSIONS: Treatment with fluvastatin ER 80 mg resulted in greater reductions in LDL-C, total cholesterol, and apo B levels compared with fluvastatin IR 40 mg, with clinically equivalent reduction in triglyceride levels and elevation of HDL-C levels. Fluvastatin 28-39 apolipoprotein B Homo sapiens 113-118 12573493-6 2003 Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species. Fluvastatin 17-28 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 38-44 12686169-7 2003 Both pravastatin (0.05 microM) and fluvastatin (0.5 microM) significantly attenuated the adhesion mediated by 27.8 mM glucose for 48 h through decreasing surface expression of endothelial adhesion molecules (intercellular adhesion molecule-1, P-selectin, and E-selectin). Fluvastatin 35-46 intercellular adhesion molecule 1 Homo sapiens 208-241 12686169-7 2003 Both pravastatin (0.05 microM) and fluvastatin (0.5 microM) significantly attenuated the adhesion mediated by 27.8 mM glucose for 48 h through decreasing surface expression of endothelial adhesion molecules (intercellular adhesion molecule-1, P-selectin, and E-selectin). Fluvastatin 35-46 selectin P Homo sapiens 243-253 12686169-7 2003 Both pravastatin (0.05 microM) and fluvastatin (0.5 microM) significantly attenuated the adhesion mediated by 27.8 mM glucose for 48 h through decreasing surface expression of endothelial adhesion molecules (intercellular adhesion molecule-1, P-selectin, and E-selectin). Fluvastatin 35-46 selectin E Homo sapiens 259-269 12573493-6 2003 Cerivastatin and fluvastatin increase CYP 2C mRNA and protein in native and cultured endothelial cells, and enhance the bradykinin-induced NO/PGI(2)-independent relaxation of arterial segments as well as the generation of reactive oxygen species. Fluvastatin 17-28 kininogen 1 Homo sapiens 120-130 14558433-8 2003 Likewise, fluconazole interferes with the CYP2C9-mediated hepatic elimination of fluvastatin. Fluvastatin 81-92 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 42-48 12588756-6 2003 Fluvastatin was also observed to enhance GTPCH and eNOS mRNA levels. Fluvastatin 0-11 GTP cyclohydrolase 1 Homo sapiens 41-46 12588757-11 2003 CONCLUSIONS: In ApoE(-/-) mice, chronic fluvastatin treatment preserved renal perfusion and vascular NO availability independently from atherosclerotic lesion prevention. Fluvastatin 40-51 apolipoprotein E Mus musculus 16-20 12515751-0 2003 Fluvastatin enhances the inhibitory effects of a selective angiotensin II type 1 receptor blocker, valsartan, on vascular neointimal formation. Fluvastatin 0-11 angiotensin II receptor type 1 Homo sapiens 59-89 12515751-3 2003 Pretreatment with fluvastatin (approximately 5 micromol/L) for 24 hours significantly inhibited Ang II (1 micromol/L)-mediated DNA synthesis and c-fos promoter activity in cultured VSMCs. Fluvastatin 18-29 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 145-150 12515751-4 2003 Moreover, pretreatment of VSMCs with fluvastatin significantly inhibited Ang II-mediated extracellular signal-regulated kinase (ERK) activation and tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3. Fluvastatin 37-48 mitogen-activated protein kinase 1 Homo sapiens 89-126 12515751-4 2003 Moreover, pretreatment of VSMCs with fluvastatin significantly inhibited Ang II-mediated extracellular signal-regulated kinase (ERK) activation and tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3. Fluvastatin 37-48 mitogen-activated protein kinase 1 Homo sapiens 128-131 12515751-4 2003 Moreover, pretreatment of VSMCs with fluvastatin significantly inhibited Ang II-mediated extracellular signal-regulated kinase (ERK) activation and tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3. Fluvastatin 37-48 signal transducer and activator of transcription 1 Homo sapiens 148-244 12515751-4 2003 Moreover, pretreatment of VSMCs with fluvastatin significantly inhibited Ang II-mediated extracellular signal-regulated kinase (ERK) activation and tyrosine- and serine-phosphorylation of signal transducer and activator of transcription (STAT)1 and STAT3. Fluvastatin 37-48 signal transducer and activator of transcription 3 Homo sapiens 249-254 12515751-5 2003 AT1 receptor-mediated recruitment of Rac-1 to Janus kinase (Jak) family/STATs was also inhibited by fluvastatin. Fluvastatin 100-111 Rac family small GTPase 1 Homo sapiens 37-42 12515751-5 2003 AT1 receptor-mediated recruitment of Rac-1 to Janus kinase (Jak) family/STATs was also inhibited by fluvastatin. Fluvastatin 100-111 signal transducer and activator of transcription 1 Homo sapiens 72-77 12515751-6 2003 Consistent with these in vitro results, phosphorylation of ERK, STAT1, and STAT3 was attenuated by the coadministration of valsartan and fluvastatin even at low doses in vivo. Fluvastatin 137-148 mitogen-activated protein kinase 1 Homo sapiens 59-62 12515751-6 2003 Consistent with these in vitro results, phosphorylation of ERK, STAT1, and STAT3 was attenuated by the coadministration of valsartan and fluvastatin even at low doses in vivo. Fluvastatin 137-148 signal transducer and activator of transcription 1 Homo sapiens 64-69 12515751-6 2003 Consistent with these in vitro results, phosphorylation of ERK, STAT1, and STAT3 was attenuated by the coadministration of valsartan and fluvastatin even at low doses in vivo. Fluvastatin 137-148 signal transducer and activator of transcription 3 Homo sapiens 75-80 12558459-7 2003 Cyclosporin-treated patients on the other hand show several-fold higher systemic exposure of all statins, both those that are metabolised by CYP3A4 and fluvastatin (metabolised by CYP2C9). Fluvastatin 152-163 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 180-186 14756189-6 2003 Fluvastatin is a statin that inhibits competitively HMGCoA reductase, like other members of this class. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 52-68 12621163-6 2003 The other HMG-CoA reductase inhibitors, atrovastatin and fluvastatin, also inhibited lysoPC-induced ERK1/2 phosphorylation. Fluvastatin 57-68 mitogen activated protein kinase 3 Rattus norvegicus 100-106 12545342-3 2003 The purpose of this study was to assess whether fluvastatin affects TAFI concentration in renal transplant recipients. Fluvastatin 48-59 carboxypeptidase B2 Homo sapiens 68-72 12545342-6 2003 TAFI and prothrombin fragments 1+2 decreased significantly after 3 months of fluvastatin administration, whereas P-selectin decreased significantly after 2 months and remained significantly lower after 3 months of this therapy. Fluvastatin 77-88 carboxypeptidase B2 Homo sapiens 0-4 12433810-2 2002 Treatment of 2- to 3-day-old human hepatocyte cultures with 3 x 10(-5) M lovastatin, simvastatin, fluvastatin, or atorvastatin for 24 h increased the amounts of CYP2B6 and CYP3A mRNA by an average of 3.8- to 9.2-fold and 24- to 36-fold, respectively. Fluvastatin 98-109 cytochrome P450 family 2 subfamily B member 6 Homo sapiens 161-167 12822205-5 2003 Fluvastatin has a low potential for drug interactions due to its CYP2C9-dependant metabolism. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 65-71 12433810-2 2002 Treatment of 2- to 3-day-old human hepatocyte cultures with 3 x 10(-5) M lovastatin, simvastatin, fluvastatin, or atorvastatin for 24 h increased the amounts of CYP2B6 and CYP3A mRNA by an average of 3.8- to 9.2-fold and 24- to 36-fold, respectively. Fluvastatin 98-109 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 172-177 12466341-0 2002 Effect of fluvastatin slow-release on low density lipoprotein (LDL) subfractions in patients with type 2 diabetes mellitus: baseline LDL profile determines specific mode of action. Fluvastatin 10-21 modular serine protease Drosophila melanogaster 63-66 12451324-11 2002 Interleukin-1beta-stimulated H-leucine incorporation was completely inhibited by fluvastatin, but not by pravastatin. Fluvastatin 81-92 interleukin 1 beta Rattus norvegicus 0-17 12466341-0 2002 Effect of fluvastatin slow-release on low density lipoprotein (LDL) subfractions in patients with type 2 diabetes mellitus: baseline LDL profile determines specific mode of action. Fluvastatin 10-21 modular serine protease Drosophila melanogaster 133-136 12466341-1 2002 The objective of this study was to determine the effect of slow-release (XL) fluvastatin on low density lipoprotein (LDL) subfractions in type 2 diabetes. Fluvastatin 77-88 modular serine protease Drosophila melanogaster 117-120 12466341-4 2002 Eight weeks of fluvastatin treatment decreased total cholesterol (-23.0%, P < 0.001), LDL-C (-29%, P < 0.001) and TG (-18%, P < 0.001), compared with placebo. Fluvastatin 15-26 component of oligomeric golgi complex 2 Homo sapiens 89-94 12466341-7 2002 Fluvastatin 80 mg XL, once daily, decreased total cholesterol and total LDL-C. Fluvastatin 0-11 component of oligomeric golgi complex 2 Homo sapiens 72-77 12480587-0 2002 [Effects of fluvastatin on the levels of C-reactive protein and lipids in patients with hyperlipidemia]. Fluvastatin 12-23 C-reactive protein Homo sapiens 41-59 12480587-1 2002 OBJECTIVE: To observe the changes of C-reactive protein (CRP) level and its relationship with blood lipids, and the effects of fluvastatin on CRP and the lipids in patients with hyperlipidemia. Fluvastatin 127-138 C-reactive protein Homo sapiens 142-145 12480587-4 2002 Fluvastatin treatment significantly reduced TC (-7.49%), TG (-14.32%), LDL (-13.88%), VLDL (-18.48%) and TC/HDL(-13.50%) levels (P<0.01), and also brought down Lp(a) concentration (-13.81%). Fluvastatin 0-11 lipoprotein(a) Homo sapiens 163-168 12480587-7 2002 Positive correlation of CRP, however, was observed after fluvastatin treatment with TC/HDL (r=0.62, P=0.041) and Lp(a) (r=0.320, P=0.011), while inverse relations were noted between CRP and HDL (r=-0.288, P=0.023). Fluvastatin 57-68 C-reactive protein Homo sapiens 24-27 12480587-9 2002 In addition to modulating blood lipid levels, fluvastatin also reduces CRP level, the latter possibly serving as an independent predictive factor for atherosclerotic cardiovascular diseases and also as an indicator for estimating the effectiveness of the treatment. Fluvastatin 46-57 C-reactive protein Homo sapiens 71-74 12466341-8 2002 In patients with atherogenic dLDL, absolute changes of dLDL were most pronounced, emphasizing the value of fluvastatin treatment in type 2 diabetes. Fluvastatin 107-118 modular serine protease Drosophila melanogaster 29-33 12208470-6 2002 Addition of fluvastatin decreased the basal and Ang II-induced IL-8 production in VSMCs in a dose (10(-8)-10(-5) mol/l)-dependent manner with a decrease in IL-8 mRNA accumulation. Fluvastatin 12-23 angiotensinogen Homo sapiens 48-54 12466341-8 2002 In patients with atherogenic dLDL, absolute changes of dLDL were most pronounced, emphasizing the value of fluvastatin treatment in type 2 diabetes. Fluvastatin 107-118 modular serine protease Drosophila melanogaster 55-59 12208470-6 2002 Addition of fluvastatin decreased the basal and Ang II-induced IL-8 production in VSMCs in a dose (10(-8)-10(-5) mol/l)-dependent manner with a decrease in IL-8 mRNA accumulation. Fluvastatin 12-23 C-X-C motif chemokine ligand 8 Homo sapiens 63-67 12208470-6 2002 Addition of fluvastatin decreased the basal and Ang II-induced IL-8 production in VSMCs in a dose (10(-8)-10(-5) mol/l)-dependent manner with a decrease in IL-8 mRNA accumulation. Fluvastatin 12-23 C-X-C motif chemokine ligand 8 Homo sapiens 156-160 12208470-7 2002 The effect of fluvastatin on IL-8 production was completely reversed in the presence of mevalonate or geranylgeranyl-pyrophosphate, but not in the presence of squalene or farnesyl-pyrophosphate. Fluvastatin 14-25 C-X-C motif chemokine ligand 8 Homo sapiens 29-33 12208470-9 2002 In conclusion, we demonstrated for the first time that Ang II increased IL-8 production and fluvastatin decreased the basal and Ang II-induced IL-8 production in human VSMCs. Fluvastatin 92-103 angiotensinogen Homo sapiens 128-134 12208470-9 2002 In conclusion, we demonstrated for the first time that Ang II increased IL-8 production and fluvastatin decreased the basal and Ang II-induced IL-8 production in human VSMCs. Fluvastatin 92-103 C-X-C motif chemokine ligand 8 Homo sapiens 143-147 12387303-1 2002 Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, and its metabolites have been reported to protect against oxidative DNA damage in vitro. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 15-62 12436350-5 2002 Fluvastatin reduced plasma levels of total cholesterol by 16%, LDL-C by 25%, and ApoB by 16% and increased plasma levels of HDL-C by 9% and apoA-1 by 7%. Fluvastatin 0-11 apolipoprotein B Homo sapiens 81-85 12436350-8 2002 There was a strong graded genotype-treatment interaction between SREBF-1a genotypes and change in apoA-I levels in response to fluvastatin (16.5% increase in GG, 10.5% in del/G, and 0.4% in del/del groups). Fluvastatin 127-138 apolipoprotein A1 Homo sapiens 98-104 12436350-9 2002 Modest interactions between SREBF-1a genotypes and changes in HDL-C, and apoC-III levels in response to fluvastatin were also present. Fluvastatin 104-115 apolipoprotein C3 Homo sapiens 73-81 12436350-12 2002 Thus we detected a strong graded interaction between SREBF-1a -36del/G genotypes and response of plasma apoA-I to treatment with fluvastatin. Fluvastatin 129-140 apolipoprotein A1 Homo sapiens 104-110 12866722-2 2002 The aim of this study was to investigate the effect of a natural statin, pravastatin, and of the synthetic one, fluvastatin, on plasma paraoxonase 1 (PON1), the antioxidant enzyme contained in plasma high-density lipoproteins. Fluvastatin 112-123 paraoxonase 1 Rattus norvegicus 135-148 12866722-2 2002 The aim of this study was to investigate the effect of a natural statin, pravastatin, and of the synthetic one, fluvastatin, on plasma paraoxonase 1 (PON1), the antioxidant enzyme contained in plasma high-density lipoproteins. Fluvastatin 112-123 paraoxonase 1 Rattus norvegicus 150-154 12866722-5 2002 Fluvastatin at a dose of 20 mg/kg/day decreased paraoxonhydrolyzing activity of PON1 by 23.6% and its phenyl acetate-hydrolyzing activity by 17.4%. Fluvastatin 0-11 paraoxonase 1 Rattus norvegicus 80-84 12866722-10 2002 These results suggest that fluvastatin but not pravastatin decreases plasma PON1 activity in normolipidemic rats, however, the former drug is more effective in reducing the level of oxidative stress. Fluvastatin 27-38 paraoxonase 1 Rattus norvegicus 76-80 12387303-6 2002 Fluvastatin and its metabolites prevented the STZ-induced elevation of DNA damage and inhibited the increase in serum levels of AST, ALT and BUN. Fluvastatin 0-11 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 128-131 12387303-6 2002 Fluvastatin and its metabolites prevented the STZ-induced elevation of DNA damage and inhibited the increase in serum levels of AST, ALT and BUN. Fluvastatin 0-11 glutamic pyruvic transaminase, soluble Mus musculus 133-136 12008961-7 2002 In vitro studies showed that the drug upregulated IkappaB alpha in unstimulated as well as in TNFalpha-stimulated cells and also impaired the TNFalpha-induced Cdc42 prenylation, indicating that fluvastatin interferes with the transcriptional activation of TF gene. Fluvastatin 194-205 tumor necrosis factor Oryctolagus cuniculus 142-150 12099998-14 2002 At a subcellular level, fluvastatin treatment was associated with reduced functional activity of Ras-dependent extracellular signal-regulated kinase pathways and of Rho-dependent p38 activation. Fluvastatin 24-35 mitogen-activated protein kinase 14 Homo sapiens 179-182 12147804-2 2002 We studied the preventive effects of a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, fluvastatin, on arterial PWV values in this population. Fluvastatin 98-109 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-86 12147804-8 2002 However, the fluvastatin group had a significantly reduced PWV (from 1991+/-162 to 1709+/-134 cm/s), oxidized LDL-C serum levels (from 89.0+/-9.6 to 73.0+/-5.8 U/l) and CRP serum levels (from 0.97+/-0.32 to 0.26+/-0.16 mg/dl) compared with those in the placebo group. Fluvastatin 13-24 C-reactive protein Homo sapiens 169-172 12374897-0 2002 Antioxidative effects of fluvastatin on superoxide anion activated by angiotensin II in human aortic smooth muscle cells. Fluvastatin 25-36 angiotensinogen Homo sapiens 70-84 12374897-1 2002 We examined the antioxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin), on superoxide anion formation activated by angiotensin II (Ang II) in vitro. Fluvastatin 41-52 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 56-103 12374897-1 2002 We examined the antioxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin), on superoxide anion formation activated by angiotensin II (Ang II) in vitro. Fluvastatin 41-52 angiotensinogen Homo sapiens 167-181 12374897-1 2002 We examined the antioxidative effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin), on superoxide anion formation activated by angiotensin II (Ang II) in vitro. Fluvastatin 41-52 angiotensinogen Homo sapiens 183-189 12374897-4 2002 hASMC treated with clinical concentrations of fluvastatin (0-100 nM) showed a dose-dependent decrease in Ang II-activated superoxide anion formation. Fluvastatin 46-57 angiotensinogen Homo sapiens 105-111 12215472-4 2002 Interestingly, antioxidants probucol and fluvastatin inhibited the oxidation of Lp(a). Fluvastatin 41-52 lipoprotein(a) Homo sapiens 80-85 12031711-1 2002 OBJECTIVE: We investigated the effects of the statins, cerivastatin and fluvastatin, on the induction of nitric oxide (NO) production in vascular smooth muscle cells (VSMC) stimulated by interleukin-1beta (IL-1) or in combination with interferon-gamma (IFN). Fluvastatin 72-83 interleukin 1 beta Homo sapiens 187-204 12044584-4 2002 In contrast, fluvastatin (mainly metabolized by CYP 2C9) and pravastatin (eliminated by other metabolic routes) are less subject to this interaction. Fluvastatin 13-24 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 48-55 11950712-0 2002 Fluvastatin reduces tissue factor expression and macrophage accumulation in carotid lesions of cholesterol-fed rabbits in the absence of lipid lowering. Fluvastatin 0-11 tissue factor Oryctolagus cuniculus 20-33 11950712-3 2002 In this study, we evaluated the ability of fluvastatin to modulate TF expression and macrophage accumulation in rabbit carotid intimal lesions independently of cholesterol lowering. Fluvastatin 43-54 tissue factor Oryctolagus cuniculus 67-69 11950712-8 2002 In the rabbits fed a high cholesterol diet without fluvastatin, an intimal lesion with macrophage accumulation and TF expression was detected. Fluvastatin 51-62 tissue factor Oryctolagus cuniculus 115-117 11950712-9 2002 Fluvastatin significantly reduced TF and macrophage content of the lesion (-50% for both). Fluvastatin 0-11 tissue factor Oryctolagus cuniculus 34-36 12008961-7 2002 In vitro studies showed that the drug upregulated IkappaB alpha in unstimulated as well as in TNFalpha-stimulated cells and also impaired the TNFalpha-induced Cdc42 prenylation, indicating that fluvastatin interferes with the transcriptional activation of TF gene. Fluvastatin 194-205 cell division control protein 42 homolog Oryctolagus cuniculus 159-164 12090904-3 2002 We investigated the effects of fluvastatin on IL-6 synthesis in human vascular smooth muscle cells (VSMCs). Fluvastatin 31-42 interleukin 6 Homo sapiens 46-50 12090904-4 2002 Addition of fluvastatin decreased IL-6 synthesis in VSMCs in a time (0-24 hours)- and dose (10(-8)-10(-5) mol/L)-dependent manner. Fluvastatin 12-23 interleukin 6 Homo sapiens 34-38 12090904-5 2002 Fluvastatin also decreased IL-6 mRNA expression in VSMCs. Fluvastatin 0-11 interleukin 6 Homo sapiens 27-31 12090904-6 2002 The effects of fluvastatin on IL-6 expression were completely reversed in the presence of mevalonate or geranylgeranyl-pyrophosphate, but not squalene. Fluvastatin 15-26 interleukin 6 Homo sapiens 30-34 12090904-8 2002 In conclusion, fluvastatin decreases IL-6 synthesis in human VSMCs through inhibition of Rho pathway. Fluvastatin 15-26 interleukin 6 Homo sapiens 37-41 11921495-0 2002 Effects of fluvastatin treatment on insulin sensitivity in patients with hyperlipidaemia. Fluvastatin 11-22 insulin Homo sapiens 36-43 11832446-7 2002 Treatment of ASPC-1 cells with fluvastatin markedly attenuated the EGF-induced translocation of RhoA from the cytosol to the membrane fraction and caused cell rounding. Fluvastatin 31-42 ras homolog family member A Homo sapiens 96-100 11779144-5 2002 Moreover, cerivastatin, fluvastatin, and pitavastatin synergistically and dose-dependently increased the transcriptional activation of PPARalpha/RXRalpha induced by bezafibrate. Fluvastatin 24-35 peroxisome proliferator activated receptor alpha Homo sapiens 135-144 11779144-5 2002 Moreover, cerivastatin, fluvastatin, and pitavastatin synergistically and dose-dependently increased the transcriptional activation of PPARalpha/RXRalpha induced by bezafibrate. Fluvastatin 24-35 retinoid X receptor alpha Homo sapiens 145-153 11854129-0 2002 Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor, attenuates left ventricular remodeling and failure after experimental myocardial infarction. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 15-62 11854129-7 2002 LV matrix metalloproteinase (MMP)-2 and MMP-13 were increased in myocardial infarction, which was attenuated in fluvastatin-treated mice. Fluvastatin 112-123 matrix metallopeptidase 2 Mus musculus 3-35 11854129-7 2002 LV matrix metalloproteinase (MMP)-2 and MMP-13 were increased in myocardial infarction, which was attenuated in fluvastatin-treated mice. Fluvastatin 112-123 matrix metallopeptidase 13 Mus musculus 40-46 11791017-4 2002 Fluvastatin but not pravastatin enhanced apoptosis in interleukin-1beta-stimulated VSMCs. Fluvastatin 0-11 interleukin 1 beta Rattus norvegicus 54-71 11791017-6 2002 Inhibition of the extracellular signal-regulated protein kinase (ERK1/2) pathway significantly increased fluvastatin-enhanced apoptosis, whereas inhibition of the p38-mitogen-activated protein kinase (MAPK) pathway significantly prevented this increase. Fluvastatin 105-116 mitogen activated protein kinase 3 Rattus norvegicus 65-71 11791017-8 2002 Furthermore, fluvastatin-induced apoptosis was inhibited by YVAD-FMK (a caspase-1/interleukin-1beta-converting enzyme-like protease inhibitor) and DEVD-FMK (a caspase-3/CPP32 inhibitor), indicating involvement of an important segment in the apoptosis signaling pathway. Fluvastatin 13-24 interleukin 1 beta Rattus norvegicus 82-99 11791017-8 2002 Furthermore, fluvastatin-induced apoptosis was inhibited by YVAD-FMK (a caspase-1/interleukin-1beta-converting enzyme-like protease inhibitor) and DEVD-FMK (a caspase-3/CPP32 inhibitor), indicating involvement of an important segment in the apoptosis signaling pathway. Fluvastatin 13-24 caspase 3 Rattus norvegicus 159-168 11791017-8 2002 Furthermore, fluvastatin-induced apoptosis was inhibited by YVAD-FMK (a caspase-1/interleukin-1beta-converting enzyme-like protease inhibitor) and DEVD-FMK (a caspase-3/CPP32 inhibitor), indicating involvement of an important segment in the apoptosis signaling pathway. Fluvastatin 13-24 caspase 3 Rattus norvegicus 169-174 11791017-9 2002 These findings suggest that fluvastatin enhances apoptosis in cytokine-stimulated VSMCs and that protein prenylation, MAPK (ERK1/2 and p38-MAPK), and caspases are critically involved in the pathways of fluvastatin-enhanced apoptosis. Fluvastatin 202-213 mitogen activated protein kinase 14 Rattus norvegicus 135-143 11774104-8 2002 There were statistically significant differences between fluvastatin and placebo treatment for the secondary outcome variables total cholesterol (-19%), triglycerides (TGs; -13%), VLDL-C (-13%), apo E (-13%), and Lp-B (-22%). Fluvastatin 57-68 apolipoprotein E Homo sapiens 195-200 12036392-9 2002 The CYP3A family metabolises lovastatin, simvastatin, atorvastatin and cerivastatin, whereas CYP2C9 metabolises fluvastatin. Fluvastatin 112-123 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 93-99 12094825-0 2002 The effect of fluvastatin on plasma fibrinogen levels. Fluvastatin 14-25 fibrinogen beta chain Homo sapiens 36-46 12094825-1 2002 There are conflicting data with regard to the effect of statins, including fluvastatin, on plasma fibrinogen levels. Fluvastatin 75-86 fibrinogen beta chain Homo sapiens 98-108 12094825-2 2002 We undertook the present study to examine the influence of fluvastatin (40 mg/day) on plasma fibrinogen levels in hypercholesterolemic non-smoker patients with normal triglyceride levels (< 2.25 mmol/l) (n = 65). Fluvastatin 59-70 fibrinogen beta chain Homo sapiens 93-103 12094825-3 2002 Fluvastatin administration was followed by a significant decrease of plasma fibrinogen levels by 8% (from 3.6 g/l to 3.33 g/l median value, p < 0.02). Fluvastatin 0-11 fibrinogen beta chain Homo sapiens 76-86 12094825-8 2002 Furthermore, in some of these studies, which Included relatively small numbers of patients, there was a trend towards a decrease in plasma fibrinogen concentration after fluvastatin administration. Fluvastatin 170-181 fibrinogen beta chain Homo sapiens 139-149 12094825-9 2002 We conclude that fluvastatin can significantly decrease plasma fibrinogen levels. Fluvastatin 17-28 fibrinogen beta chain Homo sapiens 63-73 11921495-1 2002 This study aimed to determine the effects of fluvastatin treatment on insulin sensitivity in patients with hyperlipidaemia. Fluvastatin 45-56 insulin Homo sapiens 70-77 11444504-5 2001 The lipophilic statins fluvastatin and lovastatin significantly increased interleukin-1beta-induced nitrite production by cardiac myocytes, whereas hydrophilic pravastatin did not. Fluvastatin 23-34 interleukin 1 beta Rattus norvegicus 74-91 11742861-4 2001 Cerivastatin and fluvastatin reduced the AT(1)-R mRNA and the AT(1)-R protein levels; however, pravastatin lacked this effect. Fluvastatin 17-28 angiotensin II receptor type 1 Homo sapiens 41-48 11742861-4 2001 Cerivastatin and fluvastatin reduced the AT(1)-R mRNA and the AT(1)-R protein levels; however, pravastatin lacked this effect. Fluvastatin 17-28 angiotensin II receptor type 1 Homo sapiens 62-69 11742861-5 2001 Cerivastatin and fluvastatin suppressed the AT(1)-R promoter activity measured by luciferase assay but did not affect AT(1)-R mRNA stability, suggesting that the suppression occurs at the transcriptional level. Fluvastatin 17-28 angiotensin II receptor type 1 Homo sapiens 44-51 11711273-0 2001 Secondary prevention with fluvastatin decreases levels of adhesion molecules, neopterin and C-reactive protein. Fluvastatin 26-37 C-reactive protein Homo sapiens 92-110 11907637-14 2001 Treatment with 40 mg/day fluvastatin caused a significant decrease in total cholesterol (patients: 5.47 +/- 1.32 mmol/L vs. 7.30 +/- 1.83 mmol/L; controls: 4.69 +/- 0.64 mmol/L vs. 5.81 +/- 0.72 mmol/L), LDL-C (patients: 3.28 +/- 1.25 mmol/L vs. 5.00 +/- 1.85 mmol/L; controls: 2.58 +/- 0.63 mmol/L vs. 3.50 +/- 0.70 mmol/L), and triglycerides (patients: 1.99 +/- 0.77 mmol/L vs. 2.50 +/- 1.00 mmol/L; controls: 1.24 +/- 0.46 mmol/L vs. 1.72 +/- 0.67 mmol/L) in both study groups, whereas HDL-C was not significantly changed (patients: 1.29 +/- 0.35 mmol/L vs. 1.17 +/- 0.32 mmol/L; controls: 1.55 +/- 0.30 mmol/L vs. 1.53 +/- 0.26 mmol/L). Fluvastatin 25-36 component of oligomeric golgi complex 2 Homo sapiens 204-209 11907637-23 2001 Our data suggest that fluvastatin effectively lowers plasma concentrations of cholesterol and LDL-C in patients after heart transplantation, however, the metabolism of fluvastatin is affected by concomitant therapy with cyclosporine A. Fluvastatin 22-33 component of oligomeric golgi complex 2 Homo sapiens 94-99 11762948-5 2001 RESULTS: Fluvastatin reduced, in a concentration-dependent manner (1-10 microM), the adhesion of U937 to HUVECs and the expression of E-selectin and ICAM-1 induced by anti-beta2GPI antibodies as well as by cytokines or LPS. Fluvastatin 9-20 selectin E Homo sapiens 134-144 11762948-5 2001 RESULTS: Fluvastatin reduced, in a concentration-dependent manner (1-10 microM), the adhesion of U937 to HUVECs and the expression of E-selectin and ICAM-1 induced by anti-beta2GPI antibodies as well as by cytokines or LPS. Fluvastatin 9-20 intercellular adhesion molecule 1 Homo sapiens 149-155 11762948-5 2001 RESULTS: Fluvastatin reduced, in a concentration-dependent manner (1-10 microM), the adhesion of U937 to HUVECs and the expression of E-selectin and ICAM-1 induced by anti-beta2GPI antibodies as well as by cytokines or LPS. Fluvastatin 9-20 apolipoprotein H Homo sapiens 172-180 11762948-7 2001 The inhibition of E-selectin expression exerted by fluvastatin was related to the impairment of NF-kappaB binding to DNA. Fluvastatin 51-62 selectin E Homo sapiens 18-28 11762948-7 2001 The inhibition of E-selectin expression exerted by fluvastatin was related to the impairment of NF-kappaB binding to DNA. Fluvastatin 51-62 nuclear factor kappa B subunit 1 Homo sapiens 96-105 12055702-14 2001 Pravastatin and fluvastatin significantly reduced thrombin generation only at T3 (40 mg/day); pravastatin was also associated with a decrease in LDL-C (p < 0.01, r = 0.66). Fluvastatin 16-27 coagulation factor II, thrombin Homo sapiens 50-58 11771853-3 2001 Gel retardation assay and immunocytochemical analysis of core binding factor (Cbfa1) revealed that mevastatin and fluvastatin completed the nuclear export of Cbfa1, possibly thereby reducing the induction of the stably transfected p6OSE2-luc gene, and then promoted Cbfa1-independent calcification, which invariably occurred in both wild type and dominant negative Cbfa1-expressing cells. Fluvastatin 114-125 runt related transcription factor 2 Mus musculus 78-83 11771853-3 2001 Gel retardation assay and immunocytochemical analysis of core binding factor (Cbfa1) revealed that mevastatin and fluvastatin completed the nuclear export of Cbfa1, possibly thereby reducing the induction of the stably transfected p6OSE2-luc gene, and then promoted Cbfa1-independent calcification, which invariably occurred in both wild type and dominant negative Cbfa1-expressing cells. Fluvastatin 114-125 runt related transcription factor 2 Mus musculus 158-163 11771853-3 2001 Gel retardation assay and immunocytochemical analysis of core binding factor (Cbfa1) revealed that mevastatin and fluvastatin completed the nuclear export of Cbfa1, possibly thereby reducing the induction of the stably transfected p6OSE2-luc gene, and then promoted Cbfa1-independent calcification, which invariably occurred in both wild type and dominant negative Cbfa1-expressing cells. Fluvastatin 114-125 runt related transcription factor 2 Mus musculus 158-163 11771853-3 2001 Gel retardation assay and immunocytochemical analysis of core binding factor (Cbfa1) revealed that mevastatin and fluvastatin completed the nuclear export of Cbfa1, possibly thereby reducing the induction of the stably transfected p6OSE2-luc gene, and then promoted Cbfa1-independent calcification, which invariably occurred in both wild type and dominant negative Cbfa1-expressing cells. Fluvastatin 114-125 runt related transcription factor 2 Mus musculus 158-163 11454569-0 2001 Fluvastatin inhibits O2- and ICAM-1 levels in a rat model with aortic remodeling induced by pressure overload. Fluvastatin 0-11 intercellular adhesion molecule 1 Rattus norvegicus 29-35 11454569-2 2001 The aim of the present study was to investigate the effects of the 3-hydroxy-3-methylglutaryl (HMG) CoA reductase inhibitor fluvastatin on superoxide anion (O2-) production and ICAM-1 expression in a rat model with vascular remodeling induced by pressure overload. Fluvastatin 124-135 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 67-113 11444504-6 2001 Increased nitrite production by fluvastatin was accompanied by increased iNOS mRNA and protein accumulation. Fluvastatin 32-43 nitric oxide synthase 2 Rattus norvegicus 73-77 11349008-7 2001 Heterozygous subjects had a modest reduction in HDL-C (P=0.09) and apoA1 (P=0.05) levels and a lesser response of apoA1 to treatment with fluvastatin (P=0.04). Fluvastatin 138-149 apolipoprotein A1 Homo sapiens 114-119 11406567-7 2001 Treatment of PANC-1 cells with fluvastatin markedly attenuated EGF-induced translocation of RhoA from the cytosol to the membrane fraction and actin stress fiber assembly, whereas it did not inhibit the tyrosine phosphorylation of EGF receptor and c-erbB-2. Fluvastatin 31-42 epidermal growth factor Homo sapiens 63-66 11406567-7 2001 Treatment of PANC-1 cells with fluvastatin markedly attenuated EGF-induced translocation of RhoA from the cytosol to the membrane fraction and actin stress fiber assembly, whereas it did not inhibit the tyrosine phosphorylation of EGF receptor and c-erbB-2. Fluvastatin 31-42 ras homolog family member A Homo sapiens 92-96 11406567-7 2001 Treatment of PANC-1 cells with fluvastatin markedly attenuated EGF-induced translocation of RhoA from the cytosol to the membrane fraction and actin stress fiber assembly, whereas it did not inhibit the tyrosine phosphorylation of EGF receptor and c-erbB-2. Fluvastatin 31-42 epidermal growth factor Homo sapiens 231-234 11406567-7 2001 Treatment of PANC-1 cells with fluvastatin markedly attenuated EGF-induced translocation of RhoA from the cytosol to the membrane fraction and actin stress fiber assembly, whereas it did not inhibit the tyrosine phosphorylation of EGF receptor and c-erbB-2. Fluvastatin 31-42 erb-b2 receptor tyrosine kinase 2 Homo sapiens 248-256 11406567-8 2001 The induction of cancer cell invasion by EGF was inhibited by the addition of fluvastatin or lovastatin in a dose-dependent manner. Fluvastatin 78-89 epidermal growth factor Homo sapiens 41-44 11306521-6 2001 The effect of fluvastatin on dLDL was correlated with baseline values. Fluvastatin 14-25 modular serine protease Drosophila melanogaster 29-33 11335104-0 2001 Effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on nitric oxide-induced hydroxyl radical generation in the rat heart. Fluvastatin 10-21 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 39-86 11335104-1 2001 We examined the effect of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the production of hydroxyl radical (*OH) generation via nitric oxide synthase (NOS) activation by an in vivo microdialysis technique. Fluvastatin 26-37 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 41-98 11336101-1 2001 Fluvastatin sodium (Lescol, Novartis Pharmaceutical Corp., East Hanover, NJ, U.S.A.), a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibitor that limits cholesterol biosynthesis, is available as a 40-mg immediate-release formulation capsule. Fluvastatin 0-18 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 95-153 11336101-1 2001 Fluvastatin sodium (Lescol, Novartis Pharmaceutical Corp., East Hanover, NJ, U.S.A.), a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG Co-A) reductase inhibitor that limits cholesterol biosynthesis, is available as a 40-mg immediate-release formulation capsule. Fluvastatin 20-26 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 95-153 11306521-7 2001 There was no consistent relationship, however, between the effect of fluvastatin on triglycerides and the decrease in dLDL. Fluvastatin 69-80 modular serine protease Drosophila melanogaster 118-122 11306521-8 2001 CONCLUSIONS: Fluvastatin lowers total and LDL cholesterol and the concentration of dLDL. Fluvastatin 13-24 modular serine protease Drosophila melanogaster 42-45 11306521-8 2001 CONCLUSIONS: Fluvastatin lowers total and LDL cholesterol and the concentration of dLDL. Fluvastatin 13-24 modular serine protease Drosophila melanogaster 83-87 11475198-9 2001 Interactions associated with CYP2C9-interference may, however, be present for fluvastatin. Fluvastatin 78-89 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 29-35 11181475-8 2001 Immunohistochemistry revealed that MMP-1, MMP-3, and MMP-9 expression by macrophages in the intima was lower in both the pravastatin and fluvastatin groups than in the placebo group, whereas there was no difference in macrophage numbers. Fluvastatin 137-148 interstitial collagenase Oryctolagus cuniculus 35-40 11181475-8 2001 Immunohistochemistry revealed that MMP-1, MMP-3, and MMP-9 expression by macrophages in the intima was lower in both the pravastatin and fluvastatin groups than in the placebo group, whereas there was no difference in macrophage numbers. Fluvastatin 137-148 stromelysin-1 Oryctolagus cuniculus 42-47 11181475-8 2001 Immunohistochemistry revealed that MMP-1, MMP-3, and MMP-9 expression by macrophages in the intima was lower in both the pravastatin and fluvastatin groups than in the placebo group, whereas there was no difference in macrophage numbers. Fluvastatin 137-148 matrix metalloproteinase-9 Oryctolagus cuniculus 53-58 11273020-0 2001 Antioxidative effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on peroxidation of phospholipid liposomes. Fluvastatin 24-35 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 53-100 11273020-1 2001 The antioxidative effect of fluvastatin sodium (fluvastatin), a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on lipid peroxidation of phosphatidylcholine (PC) liposomes was investigated in various peroxidizing systems. Fluvastatin 28-46 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 64-111 11273020-1 2001 The antioxidative effect of fluvastatin sodium (fluvastatin), a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on lipid peroxidation of phosphatidylcholine (PC) liposomes was investigated in various peroxidizing systems. Fluvastatin 28-39 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 64-111 11509920-1 2001 BACKGROUND: Fluvastatin is an inhibitor of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, effectively lowering serum cholesterol concentrations. Fluvastatin 12-23 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 47-104 11217077-0 2001 Protective effect of fluvastatin on degradation of apolipoprotein B by a radical reaction in human plasma. Fluvastatin 21-32 apolipoprotein B Homo sapiens 51-67 11217077-1 2001 Fluvastatin, which is a synthetic 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase inhibitor, its metabolites (M2, M3 and M4) and trolox all inhibited the decrease of apolipoprotein B-100 (apoB) and alpha-tocopherol in a radical reaction of human plasma initiated by Cu2+. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 24-89 11217077-1 2001 Fluvastatin, which is a synthetic 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase inhibitor, its metabolites (M2, M3 and M4) and trolox all inhibited the decrease of apolipoprotein B-100 (apoB) and alpha-tocopherol in a radical reaction of human plasma initiated by Cu2+. Fluvastatin 0-11 apolipoprotein B Homo sapiens 174-194 11217077-1 2001 Fluvastatin, which is a synthetic 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase inhibitor, its metabolites (M2, M3 and M4) and trolox all inhibited the decrease of apolipoprotein B-100 (apoB) and alpha-tocopherol in a radical reaction of human plasma initiated by Cu2+. Fluvastatin 0-11 apolipoprotein B Homo sapiens 196-200 11217077-2 2001 The concentrations of fluvastatin, M2, M3, M4 and trolox for 50% inhibition (IC50) of apoB fragmentation were 405, 8.55, 1.75, 305, and 43.4 microM, respectively. Fluvastatin 22-33 apolipoprotein B Homo sapiens 86-90 11286396-0 2001 Regulation of endothelial nitric oxide synthase and endothelin-1 expression by fluvastatin in human vascular endothelial cells. Fluvastatin 79-90 nitric oxide synthase 3 Homo sapiens 14-47 11286396-0 2001 Regulation of endothelial nitric oxide synthase and endothelin-1 expression by fluvastatin in human vascular endothelial cells. Fluvastatin 79-90 endothelin 1 Homo sapiens 52-64 11286396-1 2001 We investigated the effects of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on endothelial vasoactive substances using human umbilical vein endothelial cells (HUVECs). Fluvastatin 31-42 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 46-103 11286396-2 2001 Incubation of HUVECs with fluvastatin for 12 h increased endothelial nitric oxide synthase (eNOS) mRNA expression in a concentration-dependent manner (peak, 276 +/- 38%, mean +/- S.D., of the control, at 1.0 microM fluvastatin, P<0.01). Fluvastatin 26-37 nitric oxide synthase 3 Homo sapiens 57-90 11286396-4 2001 In contrast, incubation of HUVECs with 1.0 microM fluvastatin for 12 h significantly reduced the production of endothelin-1 (ET-1) and preproET-1 mRNA expression in HUVECs (28 +/- 1% and 39 +/- 1% of the control level, respectively, P<0.01). Fluvastatin 50-61 endothelin 1 Homo sapiens 111-123 11286396-4 2001 In contrast, incubation of HUVECs with 1.0 microM fluvastatin for 12 h significantly reduced the production of endothelin-1 (ET-1) and preproET-1 mRNA expression in HUVECs (28 +/- 1% and 39 +/- 1% of the control level, respectively, P<0.01). Fluvastatin 50-61 endothelin 1 Homo sapiens 125-129 11164419-3 2000 We studied in vitro the effects of fluvastatin on Th1/Th2 cytokine release in relation to caspase-1 activation, in human peripheral-blood mononuclear cells (PBMC) stimulated or not with Mycobacterium tuberculosis. Fluvastatin 35-46 negative elongation factor complex member C/D Homo sapiens 50-53 11409302-1 2001 The effect of the synthetic statin fluvastatin was investigated on the concentrations of endothelial nitric oxide synthase (eNOS) and of soluble adhesion molecules in human vascular endothelial cell cultures. Fluvastatin 35-46 nitric oxide synthase 3 Homo sapiens 89-122 11409302-3 2001 In addition, fluvastatin reduced concentrations of E-Selectin and ICAM-1. Fluvastatin 13-24 selectin E Homo sapiens 51-61 11409302-3 2001 In addition, fluvastatin reduced concentrations of E-Selectin and ICAM-1. Fluvastatin 13-24 intercellular adhesion molecule 1 Homo sapiens 66-72 11368292-13 2001 In addition to being a CYP2C9 substrate, fluvastatin demonstrates inhibitory effects on this isoenzyme in vitro and in vivo. Fluvastatin 41-52 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 23-29 11368292-14 2001 In human liver microsomes, fluvastatin significantly inhibits the hydroxylation of 2 CYP2C9 substrates, tolbutamide and diclofenac. Fluvastatin 27-38 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 85-91 11368292-15 2001 The oral clearances of the CYP2C9 substrates diclofenac, tolbutamide, glibenclamide (glyburide) and losartan are reduced by 15 to 25% when coadministered with fluvastatin. Fluvastatin 159-170 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 27-33 11164419-4 2000 Fluvastatin treatment resulted in the activation of caspase-1 and in a small secretion of interleukin (IL)-1beta, IL-18, and IFNgamma (Th1). Fluvastatin 0-11 caspase 1 Homo sapiens 52-61 11164419-4 2000 Fluvastatin treatment resulted in the activation of caspase-1 and in a small secretion of interleukin (IL)-1beta, IL-18, and IFNgamma (Th1). Fluvastatin 0-11 negative elongation factor complex member C/D Homo sapiens 135-138 11116101-5 2000 Increased nitrite production by fluvastatin was accompanied by increased iNOS mRNA and protein accumulation. Fluvastatin 32-43 nitric oxide synthase 2 Rattus norvegicus 73-77 11116101-10 2000 These results demonstrated that fluvastatin upregulates iNOS expression and subsequent NO formation in rat VSMCs through inhibition of Rho. Fluvastatin 32-43 nitric oxide synthase 2 Rattus norvegicus 56-60 10972538-2 2000 Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, has been reported to decrease the oxidizability of plasma lipids in hyperlipidaemic subjects. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 15-62 11022967-2 2000 The effects of 11 week treatments with the new hydroxy3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on renal intrinsic anti-oxidant enzyme (AOE) activities and renal function were evaluated in streptozotocin (STZ)-induced diabetic rats. Fluvastatin 112-123 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 47-101 11074211-1 2000 The purpose of this study was to determine if long-term use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (atorvastatin, fluvastatin, lovastatin, pravastatin, or simvastatin) resulted in tachyphylaxis (a decreasing response to a physiologically active agent). Fluvastatin 137-148 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 63-110 10998463-0 2000 Effect of atorvastatin and fluvastatin on the expression of plasminogen activator inhibitor type-1 in cultured human endothelial cells. Fluvastatin 27-38 serpin family E member 1 Homo sapiens 60-98 10998463-4 2000 In non-stimulated HUVEC, ATOR and FLU significantly diminished (-50% at 2.0 micromol/l) the constitutive production of PAI-1 (mRNA level and protein secretion). Fluvastatin 34-37 serpin family E member 1 Homo sapiens 119-124 10998463-7 2000 In TNFalpha-stimulated cells, ATOR and FLU had a modest down-modulating effect (-17 and -20%, respectively) on TNFalpha-induced increase in PAI-1 synthesis. Fluvastatin 39-42 tumor necrosis factor Homo sapiens 111-119 10998463-7 2000 In TNFalpha-stimulated cells, ATOR and FLU had a modest down-modulating effect (-17 and -20%, respectively) on TNFalpha-induced increase in PAI-1 synthesis. Fluvastatin 39-42 serpin family E member 1 Homo sapiens 140-145 10998463-9 2000 However, ATOR and FLU inhibited the TNFalpha-induced decrease in t-PA release. Fluvastatin 18-21 tumor necrosis factor Homo sapiens 36-44 10998463-9 2000 However, ATOR and FLU inhibited the TNFalpha-induced decrease in t-PA release. Fluvastatin 18-21 plasminogen activator, tissue type Homo sapiens 65-69 10988259-0 2000 Fluvastatin inhibits matrix metalloproteinase-1 expression in human vascular endothelial cells. Fluvastatin 0-11 matrix metallopeptidase 1 Homo sapiens 21-47 11005703-13 2000 Fluvastatin has several metabolic pathways which involve the CYP enzyme system. Fluvastatin 0-11 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 61-64 10988259-2 2000 We investigated the effects of fluvastatin on MMP-1 expression in human vascular endothelial cells (ECs). Fluvastatin 31-42 matrix metallopeptidase 1 Homo sapiens 46-51 10988259-3 2000 The addition of fluvastatin decreased the basal MMP-1 levels in the culture media of ECs in a time-dependent (0 to 48 hours) and dose-dependent (10(-)(8) to 10(-)(5) mol/L) manner. Fluvastatin 16-27 matrix metallopeptidase 1 Homo sapiens 48-53 10988259-6 2000 The effect of fluvastatin on MMP-1 expression was completely reversed in the presence of mevalonate or geranylgeranyl-pyrophosphate, but not in the presence of squalene. Fluvastatin 14-25 matrix metallopeptidase 1 Homo sapiens 29-34 10988259-8 2000 Our findings revealed that fluvastatin decreases MMP-1 expression in human vascular ECs through inhibition of Rho. Fluvastatin 27-38 matrix metallopeptidase 1 Homo sapiens 49-54 11029845-8 2000 Lovastatin, simvastatin, and atorvastatin are substrates of CYP3A4, whereas fluvastatin is metabolized by CYP2C9. Fluvastatin 76-87 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 106-112 10946846-4 2000 Moreover, the mRNA levels of p22phox, a 22-kD subunit and the protein levels of p47phox, a 47-kD subunit of nicotine adenine dinucleotide phosphate (NADPH) oxidase, was decreased by treatment with either simvastatin, fluvastatin or cerivastatin, and this effect was reversed by mevalonate, geranylgeraniol, farnesol, and cholesterol. Fluvastatin 217-228 cytochrome b-245 alpha chain Homo sapiens 29-36 11071065-0 2000 Association of the apolipoprotein B gene polymorphisms with cholesterol levels and response to fluvastatin in Brazilian individuals with high risk for coronary heart disease. Fluvastatin 95-106 apolipoprotein B Homo sapiens 19-35 10946846-4 2000 Moreover, the mRNA levels of p22phox, a 22-kD subunit and the protein levels of p47phox, a 47-kD subunit of nicotine adenine dinucleotide phosphate (NADPH) oxidase, was decreased by treatment with either simvastatin, fluvastatin or cerivastatin, and this effect was reversed by mevalonate, geranylgeraniol, farnesol, and cholesterol. Fluvastatin 217-228 neutrophil cytosolic factor 1 Homo sapiens 80-87 10928471-0 2000 Fluvastatin inhibits basal and stimulated plasminogen activator inhibitor 1, but induces tissue type plasminogen activator in cultured human endothelial cells. Fluvastatin 0-11 serpin family E member 1 Homo sapiens 42-75 11150405-2 2000 Fluvastatin is an established 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor ("statin") for the treatment of hypercholesterolemia. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 30-77 10928471-0 2000 Fluvastatin inhibits basal and stimulated plasminogen activator inhibitor 1, but induces tissue type plasminogen activator in cultured human endothelial cells. Fluvastatin 0-11 plasminogen activator, tissue type Homo sapiens 89-122 10928471-1 2000 The effects of fluvastatin, a synthetic hydroxymethylglutaryl coenzyme A (HMG-CoA) inhibitor, on the biosynthesis of tissue plasminogen activator (t-PA) and of its major physiological inhibitor (plasminogen activator inhibitor type 1, PAI-1) were investigated in cultured human umbilical vein endothelial cells (HUVEC). Fluvastatin 15-26 plasminogen activator, tissue type Homo sapiens 117-151 10928471-2 2000 Fluvastatin (0.1 to 2.5 microM), concentration-dependently reduced the release of PAI-1 antigen by unstimulated HUVEC, subsequent to a reduction in PAI-1 steady-state mRNA levels and de novo protein synthesis. Fluvastatin 0-11 serpin family E member 1 Homo sapiens 82-87 10928471-2 2000 Fluvastatin (0.1 to 2.5 microM), concentration-dependently reduced the release of PAI-1 antigen by unstimulated HUVEC, subsequent to a reduction in PAI-1 steady-state mRNA levels and de novo protein synthesis. Fluvastatin 0-11 serpin family E member 1 Homo sapiens 148-153 10928471-5 2000 Mevalonate (100 microM), a precursor of isoprenoids, added to cells simultaneously with fluvastatin, suppressed the effect of the drug on PAI-1 both in unstimulated and stimulated cells as well as on t-PA antigen. Fluvastatin 88-99 serpin family E member 1 Homo sapiens 138-143 10928471-6 2000 Among intermediates of the isoprenoid pathway, all-transgeranylgeraniol (5 microM) but not farnesol (10 microM) prevented the effect of 2.5 microM fluvastatin on PAI-1 antigen, which suggests that the former intermediate of the isoprenoid synthesis is responsible for the observed effects. Fluvastatin 147-158 serpin family E member 1 Homo sapiens 162-167 10700443-3 2000 We prospectively studied the association of the histidine (H)(72)-->tyrosine (Y) mutation in p22(phox) with the severity and progression/regression of coronary artery disease (CAD), plasma lipid levels, clinical events, and response to treatment with fluvastatin in a well-characterized population. Fluvastatin 254-265 calcineurin like EF-hand protein 1 Homo sapiens 96-99 10761170-0 2000 Flow cytometric assessment of effects of fluvastatin on low-density lipoprotein receptor activity in stimulated T-lymphocytes from patients with heterozygous familial hypercholesterolemia. Fluvastatin 41-52 low density lipoprotein receptor Homo sapiens 56-88 10761170-4 2000 Insofar that LDL receptor activity in lymphocytes reflects LDL receptor activity in the liver, the results suggest that the primary response to treatment with fluvastatin in heterozygous familial hypercholesterolemia (FH) patients is not enhanced LDL receptor activity. Fluvastatin 159-170 low density lipoprotein receptor Homo sapiens 13-25 10761170-4 2000 Insofar that LDL receptor activity in lymphocytes reflects LDL receptor activity in the liver, the results suggest that the primary response to treatment with fluvastatin in heterozygous familial hypercholesterolemia (FH) patients is not enhanced LDL receptor activity. Fluvastatin 159-170 low density lipoprotein receptor Homo sapiens 59-71 10761170-4 2000 Insofar that LDL receptor activity in lymphocytes reflects LDL receptor activity in the liver, the results suggest that the primary response to treatment with fluvastatin in heterozygous familial hypercholesterolemia (FH) patients is not enhanced LDL receptor activity. Fluvastatin 159-170 low density lipoprotein receptor Homo sapiens 59-71 10761170-5 2000 Alternatively, fluvastatin increases LDL receptor activity in hepatocytes but has little effect on receptor-dependent lipoprotein catabolism in extrahepatic tissues in vivo. Fluvastatin 15-26 low density lipoprotein receptor Homo sapiens 37-49 10780315-4 2000 RESULTS: Plasma fibrinogen significantly decreased after treatment with the combinations fluvastatin+bezafibrate (-14 and -16%) and with bezafibrate monotherapy (-9%). Fluvastatin 89-100 fibrinogen beta chain Homo sapiens 16-26 10780315-8 2000 CONCLUSIONS: The combined effects on fibrinogen and plasma lipids achieved by fluvastatin and bezafibrate combination treatment might be more useful than the simple reduction of cholesterol in preventing ischaemic cardiovascular disease. Fluvastatin 78-89 fibrinogen beta chain Homo sapiens 37-47 10952477-8 2000 The mechanism of the increased plasma concentrations and prolonged elimination of fluvastatin is probably inhibition of the CYP2C9-mediated metabolism of fluvastatin by fluconazole. Fluvastatin 82-93 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 124-130 10952477-8 2000 The mechanism of the increased plasma concentrations and prolonged elimination of fluvastatin is probably inhibition of the CYP2C9-mediated metabolism of fluvastatin by fluconazole. Fluvastatin 154-165 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 124-130 10952477-9 2000 Care should be taken if fluconazole or other potent inhibitors of CYP2C9 are prescribed to patients using fluvastatin. Fluvastatin 106-117 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 66-72 10822898-0 2000 Fluvastatin reduces soluble P-selectin and ICAM-1 levels in hypercholesterolemic patients: role of nitric oxide. Fluvastatin 0-11 selectin P Homo sapiens 28-38 10822898-0 2000 Fluvastatin reduces soluble P-selectin and ICAM-1 levels in hypercholesterolemic patients: role of nitric oxide. Fluvastatin 0-11 intercellular adhesion molecule 1 Homo sapiens 43-49 10822898-3 2000 In the present report we examined the impact of the HMG-CoA reductase inhibitor fluvastatin on plasma levels of P-selectin and ICAM-1. Fluvastatin 80-91 selectin P Homo sapiens 112-122 10822898-3 2000 In the present report we examined the impact of the HMG-CoA reductase inhibitor fluvastatin on plasma levels of P-selectin and ICAM-1. Fluvastatin 80-91 intercellular adhesion molecule 1 Homo sapiens 127-133 10822898-5 2000 RESULTS: Fluvastatin administration reduced either P-selectin (118 +/- 63 vs 81 +/- 36 ng/mL [-31%], P = 0.0015) or ICAM-1 (264 +/- 75 vs 228 +/- 68 ng/mL [-13.7%], P = 0.0033) levels. Fluvastatin 9-20 selectin P Homo sapiens 51-61 10822898-5 2000 RESULTS: Fluvastatin administration reduced either P-selectin (118 +/- 63 vs 81 +/- 36 ng/mL [-31%], P = 0.0015) or ICAM-1 (264 +/- 75 vs 228 +/- 68 ng/mL [-13.7%], P = 0.0033) levels. Fluvastatin 9-20 intercellular adhesion molecule 1 Homo sapiens 116-122 10822898-6 2000 Fluvastatin also lowered urinary 11-dehydro-TXB2 (1396 +/- 536 vs 1009 +/- 378 pg/mg creatinine [-27%], P = 0.0015) and von Willebrand Factor levels (1456 +/- 716 vs 1203 +/- 527 U/L [-17.4%], P = 0.0275), and a direct correlation was observed between P-selectin and 11-dehydro-TXB2 levels (r = 0.588, P = 0.0033). Fluvastatin 0-11 selectin P Homo sapiens 252-262 10822898-7 2000 Patients treated with fluvastatin displayed an increase in nitric oxide (NO) generation, evaluated with measurements of serum NO2-/NO3-, (4.7 +/- 1 vs 8.9 +/- 3.1) mumol/L [98%], P = 0.0046). Fluvastatin 22-33 NBL1, DAN family BMP antagonist Homo sapiens 131-134 10797611-0 2000 Lipid-lowering response of the HMG-CoA reductase inhibitor fluvastatin is influenced by polymorphisms in the low-density lipoprotein receptor gene in Brazilian patients with primary hypercholesterolemia. Fluvastatin 59-70 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 31-48 10666309-1 2000 The effects of acute treatment with fluvastatin, a hypocholesteremic drug, on the mRNA levels of several regulatory enzymes of cholesterogenesis and of the LDL receptor were determined in rat liver. Fluvastatin 36-47 low density lipoprotein receptor Rattus norvegicus 156-168 10636265-9 2000 In response to fluvastatin therapy, subjects with DD, compared with those with ID and II genotypes, had a greater reduction in total cholesterol (19% vs. 15% vs. 13%), LDL-C (31% vs. 25% vs. 21%) and apo B (23% vs. 15% vs. 12%). Fluvastatin 15-26 component of oligomeric golgi complex 2 Homo sapiens 168-173 10636265-9 2000 In response to fluvastatin therapy, subjects with DD, compared with those with ID and II genotypes, had a greater reduction in total cholesterol (19% vs. 15% vs. 13%), LDL-C (31% vs. 25% vs. 21%) and apo B (23% vs. 15% vs. 12%). Fluvastatin 15-26 apolipoprotein B Homo sapiens 200-205 10636265-12 2000 CONCLUSIONS: Angiotensin-1 converting enzyme I/D polymorphism is associated with the response of plasma lipids and coronary atherosclerosis to treatment with fluvastatin. Fluvastatin 158-169 angiotensin I converting enzyme Homo sapiens 13-44 10797611-0 2000 Lipid-lowering response of the HMG-CoA reductase inhibitor fluvastatin is influenced by polymorphisms in the low-density lipoprotein receptor gene in Brazilian patients with primary hypercholesterolemia. Fluvastatin 59-70 low density lipoprotein receptor Homo sapiens 109-141 10797611-1 2000 Although the efficacy of fluvastatin (HMG-CoA reductase inhibitor) in the treatment of primary hypercholesterolemia is well documented, a wide interindividual variation treatment response has been observed. Fluvastatin 25-36 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-55 10797611-4 2000 The results indicate that the AvaII and PvuII polymorphisms influence the cholesterol-lowering response of the HMG-CoA reductase inhibitor Fluvastatin. Fluvastatin 139-150 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 111-128 10797611-5 2000 Patients carrying A+A+ (AvaII) or P1P1 (PvuII) homozygous genotypes presented lower reduction in total cholesterol, LDL-C and apolipoprotein B levels after 16 weeks of treatment with fluvastatin, when compared to other genotypes (P<0.05). Fluvastatin 183-194 component of oligomeric golgi complex 2 Homo sapiens 116-142 10797611-7 2000 Therefore, the identification of the LDLR genetic profile may provide better prediction of a patient"s clinical response to fluvastatin. Fluvastatin 124-135 low density lipoprotein receptor Homo sapiens 37-41 10665838-9 1999 In contrast, fluvastatin (mainly metabolized by cytochrome P450-2C9) and pravastatin (eliminated by other metabolic routes) are less subject to this interaction. Fluvastatin 13-24 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 48-67 10669153-0 2000 Fluvastatin decreases soluble thrombomodulin in cardiac transplant recipients. Fluvastatin 0-11 thrombomodulin Homo sapiens 30-44 10669153-5 2000 However, fluvastatin produced a significant decrease of plasma thrombomodulin (66.7 ng/ml on placebo versus 58.8 ng/ml on fluvastatin, p <0.001), suggesting a rapid improvement of endothelial injury in these patients. Fluvastatin 9-20 thrombomodulin Homo sapiens 63-77 10575059-5 1999 The lipophilic drugs lovastatin, simvastatin, atorvastatin, cerivastatin and fluvastatin are metabolized via the cytochrome P450 (CYP450) system in the liver and the gut, making them subject to potential interactions with concomitantly administered drugs that are competing for metabolism via this system. Fluvastatin 77-88 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 113-128 10890264-2 1999 A review of the cost-effectiveness literature indicated that the hydroxymethylglutaryl coenzyme A-reductase inhibitor fluvastatin is more cost-effective for achieving minor-to-moderate reductions in low-density lipoprotein cholesterol (LDL-C) levels than 3 other statins: lovastatin, pravastatin, and simvastatin. Fluvastatin 118-129 component of oligomeric golgi complex 2 Homo sapiens 236-241 10890264-15 1999 The data showed that fluvastatin had the lowest cost-effectiveness ratios when LDL-C levels required reduction to < or =25% of baseline levels. Fluvastatin 21-32 component of oligomeric golgi complex 2 Homo sapiens 79-84 10532516-2 1999 Fluvastatin therapy was associated with a small reduction in factor VII coagulant activity, von Willebrand factor, and in plasminogen activator inhibitor 1 and tissue plasminogen activator antigens, but the effects of fluvastatin on hemostatic factors were much less marked than its effects on plasma lipids. Fluvastatin 0-11 serpin family E member 1 Homo sapiens 122-155 10532516-2 1999 Fluvastatin therapy was associated with a small reduction in factor VII coagulant activity, von Willebrand factor, and in plasminogen activator inhibitor 1 and tissue plasminogen activator antigens, but the effects of fluvastatin on hemostatic factors were much less marked than its effects on plasma lipids. Fluvastatin 0-11 chromosome 20 open reading frame 181 Homo sapiens 160-188 10651972-3 1999 Numerous studies confirm that the 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors, such as fluvastatin, are effective lipid-lowering agents in renal transplant recipients, supporting findings in other patients" groups. Fluvastatin 112-123 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 34-91 10638389-1 1999 OBJECTIVE: Fluvastatin is an agent of a new lipid lowering drug class, the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, which seems to elicit direct effects on the vasculature. Fluvastatin 11-22 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 75-122 10575059-5 1999 The lipophilic drugs lovastatin, simvastatin, atorvastatin, cerivastatin and fluvastatin are metabolized via the cytochrome P450 (CYP450) system in the liver and the gut, making them subject to potential interactions with concomitantly administered drugs that are competing for metabolism via this system. Fluvastatin 77-88 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 130-136 10513623-1 1999 Fluvastatin is a synthetic hypolipidemic drug which inhibits 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 61-118 10395027-12 1999 We found that both indomethacin and fluvastatin had an additive up-regulatory effect on LDL receptor activity. Fluvastatin 36-47 low density lipoprotein receptor Homo sapiens 88-100 10515287-2 1999 Treatment with the HMG-CoA-reductase inhibitor fluvastatin (40 mg) significantly reduced the serum low density lipoprotein cholesterol concentration by 30% (p<0.01) and total cholesterol by 25% (p<0.01). Fluvastatin 47-58 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 19-36 10515287-3 1999 The platelet membrane activation markers CD62 (PADGEM, P-selectin, GMP140) and 63 (GP53) significantly decreased by 22 and 13% (in terms of the relative fluorescence intensity) under the treatment with fluvastatin (p<0.05), respectively. Fluvastatin 202-213 selectin P Homo sapiens 41-45 10515287-3 1999 The platelet membrane activation markers CD62 (PADGEM, P-selectin, GMP140) and 63 (GP53) significantly decreased by 22 and 13% (in terms of the relative fluorescence intensity) under the treatment with fluvastatin (p<0.05), respectively. Fluvastatin 202-213 selectin P Homo sapiens 55-65 10515287-3 1999 The platelet membrane activation markers CD62 (PADGEM, P-selectin, GMP140) and 63 (GP53) significantly decreased by 22 and 13% (in terms of the relative fluorescence intensity) under the treatment with fluvastatin (p<0.05), respectively. Fluvastatin 202-213 selectin P Homo sapiens 67-73 11245097-1 1999 AIM: To evaluate the effects of fluvastatin, a hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor, on the alterations of structure and function of resistant vessels in spontaneously hypertensive rats (SHR). Fluvastatin 32-43 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 47-92 10434403-1 1999 We investigated the in vitro hydroxyl radical scavenging activity of fluvastatin, a 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor. Fluvastatin 69-80 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 84-130 10434403-3 1999 Since this effect was not observed in other HMG-CoA reductase inhibitors, such as pravastatin and simvastatin, the scavenging effect of fluvastatin on hydroxyl radicals would not be a common property of HMG-CoA reductase inhibitors, but is derived from the unique chemical structure of fluvastatin. Fluvastatin 136-147 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 44-61 10434403-3 1999 Since this effect was not observed in other HMG-CoA reductase inhibitors, such as pravastatin and simvastatin, the scavenging effect of fluvastatin on hydroxyl radicals would not be a common property of HMG-CoA reductase inhibitors, but is derived from the unique chemical structure of fluvastatin. Fluvastatin 136-147 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 203-220 10381298-6 1999 Fluvastatin treatment for 52 weeks was associated with a 24.2% reduction in LDL-cholesterol (P < 0.001) as well as a 40.7% decrease in the expression density of CD14 on all monocytes (P = 0.027). Fluvastatin 0-11 CD14 molecule Homo sapiens 164-168 10381298-8 1999 The positive pre-study correlation of the CD14dimCD16+ monocyte subset to the serum cholesterol concentration, but inverse changes of both parameters under fluvastatin therapy, in conclusion indicate that fluvastatin exerts an as yet uncharacterized immunomodulatory effect on either monocyte maturation and differentiation, or extravasation which may also depend on the endothelial phenotype that is independent of the change in serum lipids. Fluvastatin 205-216 CD14 molecule Homo sapiens 42-53 10197301-0 1999 The effects of fluvastatin, a CYP2C9 inhibitor, on losartan pharmacokinetics in healthy volunteers. Fluvastatin 15-26 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 30-36 10323270-3 1999 We found that the addition of serum from patients treated with fluvastatin for 6 days caused a significant reduction in cell proliferation, increased cell apoptosis and reduced the B cell leukemia-2 (bcl-2) concentration. Fluvastatin 63-74 BCL2 apoptosis regulator Homo sapiens 181-198 10323270-3 1999 We found that the addition of serum from patients treated with fluvastatin for 6 days caused a significant reduction in cell proliferation, increased cell apoptosis and reduced the B cell leukemia-2 (bcl-2) concentration. Fluvastatin 63-74 BCL2 apoptosis regulator Homo sapiens 200-205 10357007-0 1999 Increasing plasma fibrinogen, but unchanged levels of intraplatelet cyclic nucleotides, plasma endothelin-1, factor VII, and neopterin during cholesterol lowering with fluvastatin. Fluvastatin 168-179 fibrinogen beta chain Homo sapiens 18-28 10357007-7 1999 In conclusion, during cholesterol-lowering treatment with fluvastatin, plasma levels of fibrinogen increased whereas intraplatelet cyclic nucleotide levels and plasma endothelin-1, factor VII and neopterin levels were unchanged. Fluvastatin 58-69 fibrinogen beta chain Homo sapiens 88-98 10037456-0 1999 Protective effect of fluvastatin sodium (XU-62-320), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on oxidative modification of human low-density lipoprotein in vitro. Fluvastatin 21-39 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 55-112 10037456-0 1999 Protective effect of fluvastatin sodium (XU-62-320), a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on oxidative modification of human low-density lipoprotein in vitro. Fluvastatin 41-50 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 55-112 9922713-1 1999 Fluvastatin (FV) is a highly potent inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 49-99 10064574-0 1999 The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin: effect on human cytochrome P-450 and implications for metabolic drug interactions. Fluvastatin 62-73 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-51 10064574-0 1999 The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin: effect on human cytochrome P-450 and implications for metabolic drug interactions. Fluvastatin 62-73 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 91-107 10064574-1 1999 Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, was metabolized by human liver microsomes to 5-hydroxy-, 6-hydroxy-, and N-deisopropyl-fluvastatin. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 15-62 10064574-3 1999 Several enzymes, but mainly CYP2C9, catalyzed fluvastatin metabolism. Fluvastatin 46-57 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 28-34 10064574-6 1999 Fluvastatin in turn inhibited CYP2C9-catalyzed tolbutamide and diclofenac hydroxylation with Ki values of 0.3 and 0.5 microM, respectively. Fluvastatin 0-11 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 30-36 10064574-7 1999 For CYP2C8-catalyzed 6alpha-hydroxy-paclitaxel formation the IC50 was 20 microM and for CYP1A2, CYP2C19, and CYP3A catalyzed reactions, no IC50 could be determined up to 100 microM fluvastatin. Fluvastatin 181-192 cytochrome P450 family 2 subfamily C member 8 Homo sapiens 4-10 10064574-8 1999 All three fluvastatin metabolites were also formed by recombinant CYP2C9, whereas CYP1A1, CYP2C8, CYP2D6, and CYP3A4 produced only 5-hydroxy-fluvastatin. Fluvastatin 10-21 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 66-72 10064574-8 1999 All three fluvastatin metabolites were also formed by recombinant CYP2C9, whereas CYP1A1, CYP2C8, CYP2D6, and CYP3A4 produced only 5-hydroxy-fluvastatin. Fluvastatin 10-21 cytochrome P450 family 1 subfamily A member 1 Homo sapiens 82-88 10064574-12 1999 This data indicates that several human cytochrome P-450 enzymes metabolize fluvastatin with CYP2C9 contributing 50-80%. Fluvastatin 75-86 cytochrome P450 family 4 subfamily F member 3 Homo sapiens 39-55 10064574-12 1999 This data indicates that several human cytochrome P-450 enzymes metabolize fluvastatin with CYP2C9 contributing 50-80%. Fluvastatin 75-86 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 92-98 10355866-4 1999 Soluble P-selectin (sP-selectin) levels were significantly lowered after 12 weeks of fluvastatin treatment (157.0 ng/ml versus 113.77 ng/ml, p = 0.01), whereas 12 weeks of placebo treatment had no statistically significant effect on sP-selectin levels (150.0 ng/ml versus 139.4 ng/ml). Fluvastatin 85-96 selectin P Homo sapiens 8-18 10355866-7 1999 By lowering the levels of P-selectin, fluvastatin may not only attenuate atherosclerotic progression but may also decrease the platelet activation associated with PAOD. Fluvastatin 38-49 selectin P Homo sapiens 26-36 9922713-1 1999 Fluvastatin (FV) is a highly potent inhibitor of 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase. Fluvastatin 13-15 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 49-99 9825814-7 1998 RESULTS: After 8 weeks of treatment with a dose of fluvastatin necessary to reduce LDL-C below 3.5 mmol/L (20 mg for 3 and 40 mg for 16 patients), total cholesterol was lowered by 20% and LDL-C by 30%, and HDL2-C was increased by 35% (all P<0.01). Fluvastatin 51-62 junctophilin 3 Homo sapiens 206-210 9812903-4 1998 We studied the effect of fluvastatin on the activity of MMP-9 in mouse and human macrophages in culture. Fluvastatin 25-36 matrix metallopeptidase 9 Mus musculus 56-61 9812903-6 1998 In mouse macrophages, fluvastatin (5 to 100 micromol/L) significantly inhibited in a dose-dependent manner MMP-9 activity from 20% to 40% versus control. Fluvastatin 22-33 matrix metallopeptidase 9 Mus musculus 107-112 9571146-1 1998 We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT. Fluvastatin 50-61 kininogen 1 Homo sapiens 65-75 9793596-12 1998 In comparison, currently available HMG-CoA reductase inhibitors (lovastatin, simvastatin, pravastatin, fluvastatin, cerivastatin) lower LDL-C concentrations by approximately 20-40% and TG concentrations by approximately 10-30%. Fluvastatin 103-114 component of oligomeric golgi complex 2 Homo sapiens 136-141 10076536-8 1998 The concentrations of several glucocorticoids that produced suppression of Fluva-induced CYP2B1/2 mRNA levels were the same concentrations that induced CYP3A mRNA. Fluvastatin 75-80 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 89-95 10076536-8 1998 The concentrations of several glucocorticoids that produced suppression of Fluva-induced CYP2B1/2 mRNA levels were the same concentrations that induced CYP3A mRNA. Fluvastatin 75-80 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 152-157 10076536-9 1998 Treatment with pregnenolone 16 alpha-carbonitrile also produced a concentration-dependent suppression of Fluva-induced CYP2B1/2 mRNA levels. Fluvastatin 105-110 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 119-125 10076536-10 1998 Dex-mediated suppression of Fluva-induced CYP2B1/2 mRNA was concentration-dependently reversed when hepatocytes were cotreated with troleandomycin, a selective CYP3A inhibitor. Fluvastatin 28-33 cytochrome P450, family 2, subfamily b, polypeptide 12 Rattus norvegicus 42-50 10076536-10 1998 Dex-mediated suppression of Fluva-induced CYP2B1/2 mRNA was concentration-dependently reversed when hepatocytes were cotreated with troleandomycin, a selective CYP3A inhibitor. Fluvastatin 28-33 cytochrome P450, family 3, subfamily a, polypeptide 62 Rattus norvegicus 160-165 10076536-12 1998 However, Dex-mediated suppression of Fluva-induced CYP2B1/2 mRNA expression was not overcome when hepatocytes were incubated with Fluva concentrations greater than 3 x 10(-5) M, suggesting that mechanisms other than CYP3A-catalyzed metabolism may contribute to Dex-mediated suppression of Fluva-induced CYP2B1/2 expression. Fluvastatin 37-42 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 51-57 10076536-12 1998 However, Dex-mediated suppression of Fluva-induced CYP2B1/2 mRNA expression was not overcome when hepatocytes were incubated with Fluva concentrations greater than 3 x 10(-5) M, suggesting that mechanisms other than CYP3A-catalyzed metabolism may contribute to Dex-mediated suppression of Fluva-induced CYP2B1/2 expression. Fluvastatin 37-42 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 303-309 9804052-5 1998 In the treatment of transplant patients, from a drug interaction perspective, pravastatin, which is not significantly metabolized by CYP enzymes, and fluvastatin, presumably a CYP2C9 substrate, compare favorably with the other statins for which the major metabolic pathways are catalyzed by CYP3A. Fluvastatin 150-161 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 176-182 10076536-1 1998 Fluvastatin (Fluva), a synthetic inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, induces CYP2B1/2 in rat liver and primary cultured rat hepatocytes. Fluvastatin 0-11 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 103-109 10076536-1 1998 Fluvastatin (Fluva), a synthetic inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, induces CYP2B1/2 in rat liver and primary cultured rat hepatocytes. Fluvastatin 0-5 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 103-109 10076536-5 1998 Only dexamethasone (Dex) produced effects on Fluva-inducible CYP2B1/2 mRNA expression that differed from those produced on PB-inducible CYP2B1/2 mRNA expression. Fluvastatin 45-50 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 61-67 9571146-1 1998 We analyzed the effect of isoprenoid depletion by fluvastatin on bradykinin (BK)- and epidermal growth factor (EGF)-mediated Ca2+ mobilization and prostaglandin E2 production, in the human keratinocyte cell line HaCaT. Fluvastatin 50-61 kininogen 1 Homo sapiens 77-79 9349932-3 1997 It was of interest to determine whether lipid-lowering therapy with fluvastatin, a potent HMGCoA reductase inhibitor, affected LDL oxidation and trace metal levels. Fluvastatin 68-79 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 90-106 18020528-4 1997 The hydrophilic HMG-CoA reductase inhibitors, such as pravastatin and fluvastatin, should be distinguished from the lipophilic agents, lovastatin and simvastatin, with regard to toxicity and accumulation. Fluvastatin 70-81 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 16-33 9328321-9 1997 The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin reverses the inhibitory effect of both hydrocortisone and cyclosporine. Fluvastatin 72-83 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 4-61 9271817-10 1997 The reported reduction of TFPI antigen levels after fluvastatin treatment could be a sign of normalization of an up-regulated clotting system rather than an unfavourable reduction of a natural anticoagulant. Fluvastatin 52-63 tissue factor pathway inhibitor Homo sapiens 26-30 9301630-1 1997 The overall objective of this study was to determine whether peroral treatment with the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin influences the leukocyte-endothelial cell adhesion (LECA) observed in postcapillary venules of hypercholesterolemic rats. Fluvastatin 157-168 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 88-146 9081680-6 1997 The inhibitory effect of fluvastatin on TF activity and antigen was fully reversible by coincubation with 100 mumol/L mevalonate or 10 mumol/L all-trans-geranylgeraniol but not with dolichol, farnesol, or geraniol. Fluvastatin 25-36 coagulation factor III, tissue factor Homo sapiens 40-42 9081680-8 1997 Furthermore, fluvastatin impaired bacterial lipopolysaccharide-induced binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter, indicating that this drug influences induction of the TF gene. Fluvastatin 13-24 REL proto-oncogene, NF-kB subunit Homo sapiens 82-87 9081680-8 1997 Furthermore, fluvastatin impaired bacterial lipopolysaccharide-induced binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter, indicating that this drug influences induction of the TF gene. Fluvastatin 13-24 RELA proto-oncogene, NF-kB subunit Homo sapiens 88-91 9081680-8 1997 Furthermore, fluvastatin impaired bacterial lipopolysaccharide-induced binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter, indicating that this drug influences induction of the TF gene. Fluvastatin 13-24 coagulation factor III, tissue factor Homo sapiens 130-132 9081680-8 1997 Furthermore, fluvastatin impaired bacterial lipopolysaccharide-induced binding of c-Rel/p65 heterodimers to a kappa B site in the TF promoter, indicating that this drug influences induction of the TF gene. Fluvastatin 13-24 coagulation factor III, tissue factor Homo sapiens 197-199 9025904-6 1997 Brefeldin A (BFA), colchicine, and the HMGCoA-reductase inhibitor fluvastatin disrupted the characteristic Golgi localization of IL-8, but only BFA inhibited its secretion. Fluvastatin 66-77 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-55 9025904-6 1997 Brefeldin A (BFA), colchicine, and the HMGCoA-reductase inhibitor fluvastatin disrupted the characteristic Golgi localization of IL-8, but only BFA inhibited its secretion. Fluvastatin 66-77 C-X-C motif chemokine ligand 8 Homo sapiens 129-133 9509899-1 1998 The recent development of specific competitive inhibitors of the hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase such as lovastatin, simvastatin, pravastatin and fluvastatin has provided an important new and effective approach to the treatment of hyperlipidaemia and atherosclerosis. Fluvastatin 167-178 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 65-117 9377621-6 1997 Fluvastatin 20 mg/d reduced low-density lipoprotein cholesterol (LDL-C) levels by 21.0% and total cholesterol (total-C) levels by 16.4%; fluvastatin 40 mg/d reduced these levels by 23.1% and 17.7%, respectively. Fluvastatin 0-11 component of oligomeric golgi complex 2 Homo sapiens 28-63 9377621-6 1997 Fluvastatin 20 mg/d reduced low-density lipoprotein cholesterol (LDL-C) levels by 21.0% and total cholesterol (total-C) levels by 16.4%; fluvastatin 40 mg/d reduced these levels by 23.1% and 17.7%, respectively. Fluvastatin 0-11 component of oligomeric golgi complex 2 Homo sapiens 65-70 9096917-0 1997 Efficacy and safety of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor fluvastatin in hyperlipidemic patients treated with probucol. Fluvastatin 85-96 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 27-74 9096917-1 1997 The objective of this open trial was to investigate the efficacy and safety of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin in hypercholesterolemic patients already receiving probucol. Fluvastatin 151-162 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 83-140 9096917-9 1997 In addition, fluvastatin significantly decreased serum apolipoprotein B, C-II, C-III and E levels, whereas serum apolipoprotein A-I and A-II levels were unaffected. Fluvastatin 13-24 apolipoprotein B Homo sapiens 55-71 9081680-2 1997 We examined the effect of fluvastatin, the first entirely synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor that is structurally different from other vastatins, on tissue factor (TF) expression in human macrophages spontaneously differentiated in culture from blood monocytes. Fluvastatin 26-37 coagulation factor III, tissue factor Homo sapiens 182-195 9081680-2 1997 We examined the effect of fluvastatin, the first entirely synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor that is structurally different from other vastatins, on tissue factor (TF) expression in human macrophages spontaneously differentiated in culture from blood monocytes. Fluvastatin 26-37 coagulation factor III, tissue factor Homo sapiens 197-199 9081680-3 1997 Fluvastatin decreased TF activity in a dose-dependent manner (1 to 5 mumol/L) in both unstimulated and lipopolysaccharide-stimulated macrophages, and this reduction paralleled the decrease in immunologically recognized TF protein. Fluvastatin 0-11 coagulation factor III, tissue factor Homo sapiens 22-24 9081680-3 1997 Fluvastatin decreased TF activity in a dose-dependent manner (1 to 5 mumol/L) in both unstimulated and lipopolysaccharide-stimulated macrophages, and this reduction paralleled the decrease in immunologically recognized TF protein. Fluvastatin 0-11 coagulation factor III, tissue factor Homo sapiens 219-221 9089010-3 1996 Fluvastatin at 0.1 microM or more inhibited the expression of lymphocyte function associated antigen-1 (LFA-1) on U937 and intercellular adhesion molecule-1 (ICAM-1) on U937. Fluvastatin 0-11 integrin subunit alpha L Homo sapiens 62-102 8941022-1 1996 OBJECTIVES: The primary objective was to investigate the effective permeability and the hepatic extraction of fluvastatin, a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, during a jejunal perfusion in humans. Fluvastatin 110-121 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 129-186 8937733-0 1996 Inhibitory effects of fluvastatin, a new HMG-CoA reductase inhibitor, on the increase in vascular ACE activity in cholesterol-fed rabbits. Fluvastatin 22-33 angiotensin-converting enzyme Oryctolagus cuniculus 98-101 8937733-2 1996 The effects of fluvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the vascular angiotensin converting enzyme (ACE) activity in hyperlipidaemic rabbits were compared with those of enalapril, an ACE inhibitor. Fluvastatin 15-26 angiotensin-converting enzyme Oryctolagus cuniculus 119-148 8937733-2 1996 The effects of fluvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the vascular angiotensin converting enzyme (ACE) activity in hyperlipidaemic rabbits were compared with those of enalapril, an ACE inhibitor. Fluvastatin 15-26 angiotensin-converting enzyme Oryctolagus cuniculus 150-153 8937733-9 1996 Fluvastatin as well as enalapril significantly lowered the tissue ACE in the aortae. Fluvastatin 0-11 angiotensin-converting enzyme Oryctolagus cuniculus 66-69 8937733-20 1996 Thus, the decrease in vascular ACE activity by fluvastatin as well as the lipid-lowering effect may reduce the risk of atherosclerosis progression in the vasculature. Fluvastatin 47-58 angiotensin-converting enzyme Oryctolagus cuniculus 31-34 8937853-3 1996 Treatment of cultured hepatocytes with lovastatin, simvastatin, or fluvastatin increased CYP2B1/2, CYP3A1/2, and CYP4A mRNA and immunoreactive protein levels over the dose range (3 x 10(-6) to 3 x 10(-5) M) required to increase the amount of HMG-CoA reductase mRNA. Fluvastatin 67-78 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 89-95 8937853-3 1996 Treatment of cultured hepatocytes with lovastatin, simvastatin, or fluvastatin increased CYP2B1/2, CYP3A1/2, and CYP4A mRNA and immunoreactive protein levels over the dose range (3 x 10(-6) to 3 x 10(-5) M) required to increase the amount of HMG-CoA reductase mRNA. Fluvastatin 67-78 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 99-107 8937853-4 1996 The increases in CYP2B1/2 levels produced by 3 x 10(-5) M fluvastatin treatment were larger than those produced by lovastatin or simvastatin treatment or by treatment with 10(-4) M phenobarbital. Fluvastatin 58-69 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 17-23 8937853-5 1996 In contrast, treatment of cultured hepatocytes with 3 x 10(-5) M lovastatin, simvastatin, or fluvastatin increased CYP3A1/2 and CYP4A mRNA and immunoreactive protein to lower levels than those produced by treatment with 10(-5) M dexamethasone or 10(-4) M ciprofibrate. Fluvastatin 93-104 cytochrome P450, family 3, subfamily a, polypeptide 23-polypeptide 1 Rattus norvegicus 115-121 8937853-7 1996 Incubation of hepatocytes with 10(-4) M fluvastatin increased CYP1A1 mRNA to 67% of the level induced by treatment with 10(-5) M beta-naphthoflavone. Fluvastatin 40-51 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 62-68 8937853-8 1996 Doses of 50 or 100 mg/ kg/day fluvastatin administered for 3 days to rats increased the hepatic levels of CYP2B1/2 and CYP4A mRNA and immunoreactive protein, although to much lower levels than those produced by treatment with phenobarbital or ciprofibrate, respectively. Fluvastatin 30-41 cytochrome P450, family 2, subfamily b, polypeptide 1 Rattus norvegicus 106-112 8937853-10 1996 However, treatment with 50 mg/kg/day fluvastatin induced CYP1A1 mRNA and protein. Fluvastatin 37-48 cytochrome P450, family 1, subfamily a, polypeptide 1 Rattus norvegicus 57-63 9089010-3 1996 Fluvastatin at 0.1 microM or more inhibited the expression of lymphocyte function associated antigen-1 (LFA-1) on U937 and intercellular adhesion molecule-1 (ICAM-1) on U937. Fluvastatin 0-11 integrin subunit alpha L Homo sapiens 104-109 9089010-3 1996 Fluvastatin at 0.1 microM or more inhibited the expression of lymphocyte function associated antigen-1 (LFA-1) on U937 and intercellular adhesion molecule-1 (ICAM-1) on U937. Fluvastatin 0-11 intercellular adhesion molecule 1 Homo sapiens 123-156 9089010-3 1996 Fluvastatin at 0.1 microM or more inhibited the expression of lymphocyte function associated antigen-1 (LFA-1) on U937 and intercellular adhesion molecule-1 (ICAM-1) on U937. Fluvastatin 0-11 intercellular adhesion molecule 1 Homo sapiens 158-164 8927338-12 1996 In Group B fluvastatin significantly reduced the level of TC (from 7.22 +/- 0.88 to 5.99 +/- 0.98 mM/L), of LDL-C (from 5.13 +/- 0.71 to 3.95 +/- 0.88 mM/L), and the level of ApoB (from 0.97 +/- 0.26 to 0.85 +/- 0.15 mM/L), but did not influence significantly the level of HDL-C, ApoA1 and TG. Fluvastatin 11-22 apolipoprotein B Homo sapiens 175-179 8927338-12 1996 In Group B fluvastatin significantly reduced the level of TC (from 7.22 +/- 0.88 to 5.99 +/- 0.98 mM/L), of LDL-C (from 5.13 +/- 0.71 to 3.95 +/- 0.88 mM/L), and the level of ApoB (from 0.97 +/- 0.26 to 0.85 +/- 0.15 mM/L), but did not influence significantly the level of HDL-C, ApoA1 and TG. Fluvastatin 11-22 apolipoprotein A1 Homo sapiens 280-285 8630058-3 1996 Indirect inhibition of prenylation with the HMG CoA reductase inhibitors fluvastatin or compactin decreased bradykinin-stimulated inositol 1,4,5-triphosphate generation. Fluvastatin 73-84 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 44-61 8630058-3 1996 Indirect inhibition of prenylation with the HMG CoA reductase inhibitors fluvastatin or compactin decreased bradykinin-stimulated inositol 1,4,5-triphosphate generation. Fluvastatin 73-84 kininogen 1 Homo sapiens 108-118 8561503-3 1996 We found that administration of inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase such as lovastatin, pravastatin, fluvastatin, and rivastatin resulted in increased hepatic LDL receptor mRNA levels. Fluvastatin 127-138 low density lipoprotein receptor Rattus norvegicus 185-197 7670949-3 1995 Our results indicate that the HMG-CoA reductase inhibitors fluvastatin and simvastatin reduce, in a concentration-dependent manner, more than 50% of the 125I-AcLDL degradation by macrophages. Fluvastatin 59-70 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 30-47 7570971-5 1995 After 12 weeks of treatment, fluvastatin 20 mg significantly reduced TC by 13.4% (from 6.7 +/- 0.5 [mean +/- SEM] to 5.8 +/- 0.2 mmol/L), LDL-C by 22% (from 4.1 +/- 0.3 to 3.2 +/- 0.2 mmol/L), and Apo B by 13.2% (from 159.6 +/- 8.8 to 138.6 +/- 9.2 mg/dl) (P < 0.005). Fluvastatin 29-40 apolipoprotein B Homo sapiens 197-202 7570971-6 1995 The subsequent 12-week treatment of fluvastatin 40 mg significantly reduced TC by 16.4% to 5.6 +/- 0.3 mmol/L, LDL-C by 29.3% to 2.9 +/- 0.2 mmol/L, and Apo B by 18.2% to 130.6 +/- 5.5 mg/dl (P < 0.00005). Fluvastatin 36-47 apolipoprotein B Homo sapiens 153-158 8729587-12 1996 An open-label ongoing study on a larger cohort of FH patients reveals that a decrease in plasma LDL-C levels of up to 38.5% may be achieved with a combination of fluvastatin 80 mg/day and bezafibrate 400 mg/day. Fluvastatin 162-173 component of oligomeric golgi complex 2 Homo sapiens 96-101 8729588-1 1996 Fluvastatin, a new synthetic inhibitor of HMGCoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, has been studied in several models to examine its effects when used in combination with other lipid-modifying agents such as derivatives of fibric acid (bezafibrate), resins (cholestyramine), and niacin. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 50-98 8729591-8 1996 Our group has studied the short- and long-term effect of fluvastatin on Lp(a) in hypercholesterolaemic patients; fluvastatin was found to have no effect in such patients as observed in the short-term studies, but significant reductions in Lp(a) levels were noted during long-term treatment. Fluvastatin 57-68 lipoprotein(a) Homo sapiens 72-77 8737761-6 1996 CONCLUSION: Fluvastatin selectively inhibits a major drug metabolising enzyme (CYP2C9), the (+)-isomer (pharmacologically more active) showing 4-5 fold higher affinity. Fluvastatin 12-23 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 79-85 8773189-3 1995 There was a concentration dependent decrease in the proliferation of human and porcine SMC, when cells were incubated in the presence of fluvastatin, a new, fully synthetic HMGCoA-reductase inhibitor. Fluvastatin 137-148 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 173-189 8773189-8 1995 This indicates that the inhibitory effect of fluvastatin is caused by the inhibition of HMGCoA-reductase and depletion of mevalonate rather than being unspecific. Fluvastatin 45-56 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 88-104 8773189-12 1995 HMGCoA-reductase inhibitors like fluvastatin block the synthesis of these nonsterol precursors in human and porcine vascular SMC in vitro and are therefore growth inhibitory. Fluvastatin 33-44 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 0-16 7492622-0 1995 High dose of fluvastatin sodium (XU62-320), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, lowers plasma cholesterol levels in homozygous Watanabe-heritable hyperlipidemic rabbits. Fluvastatin 13-31 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 63-110 7492622-1 1995 The effects of fluvastatin sodium (XU62-320), a new type of inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on plasma cholesterol and triacylglycerol levels were investigated using homozygous Watanabe-heritable hyperlipidemic (WHHL) rabbit, an LDL-receptor-deficient animal which expresses a hepatic LDL receptor activity less than 5% that of control rabbits. Fluvastatin 15-33 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 73-120 7492622-5 1995 Combined administration of fluvastatin (50 mg/kg per day) and cholestyramine, a bile acid sequestrant resin, at a level of 2% of the diet for 4 weeks more profoundly decreased plasma total, VLDL- and LDL-cholesterol levels with induction of hepatic cholesterol 7 alpha-hydroxylase and no further induction of the hepatic LDL receptor. Fluvastatin 27-38 cytochrome P450 7A1 Oryctolagus cuniculus 249-280 7492622-5 1995 Combined administration of fluvastatin (50 mg/kg per day) and cholestyramine, a bile acid sequestrant resin, at a level of 2% of the diet for 4 weeks more profoundly decreased plasma total, VLDL- and LDL-cholesterol levels with induction of hepatic cholesterol 7 alpha-hydroxylase and no further induction of the hepatic LDL receptor. Fluvastatin 27-38 low-density lipoprotein receptor Oryctolagus cuniculus 321-333 7492622-7 1995 These results suggest that high dose of fluvastatin sodium is effective in lowering plasma cholesterol levels in homozygous WHHL rabbits through the shared mechanisms involving decrease in production and secretion of cholesterol from the liver and the induction of hepatic LDL receptor. Fluvastatin 40-58 low-density lipoprotein receptor Oryctolagus cuniculus 273-285 7586933-0 1995 In vivo inhibition profile of cytochrome P450TB (CYP2C9) by (+/-)-fluvastatin. Fluvastatin 60-77 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 49-55 7586933-1 1995 BACKGROUND: (+/-)-Fluvastatin is a synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor that selectively and competitively inhibits P450TB (CYP2C9) in vitro. Fluvastatin 12-29 cytochrome P450 family 2 subfamily C member 9 Homo sapiens 165-171 7670949-8 1995 Studies performed with native 125I-LDL indicated that fluvastatin did not inhibit but rather increased the degradation of LDL taken up by the normal LDL receptor. Fluvastatin 54-65 low density lipoprotein receptor Mus musculus 149-161 7604786-11 1995 In conclusion, LDL-C lowering with short-term fluvastatin therapy improved myocardial perfusion, especially in areas of ischemia. Fluvastatin 46-57 component of oligomeric golgi complex 2 Homo sapiens 15-20 7604789-4 1995 Total cholesterol, low density lipoprotein cholesterol, and apolipoprotein (apo) B were each reduced to the same extent with the 2 doses of fluvastatin (-20%, -26%, and -20%, respectively). Fluvastatin 140-151 apolipoprotein B Homo sapiens 60-82 7604781-2 1995 We therefore studied the safety and efficacy of the hydrophilic HMG-CoA reductase inhibitor fluvastatin in 14 cyclosporine-treated renal transplant patients. Fluvastatin 92-103 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 64-81 7604797-0 1995 Clinical efficacy of fluvastatin in the long-term treatment of familial hypercholesterolemia. Fluvastatin 21-32 low density lipoprotein receptor Homo sapiens 63-92 7604781-12 1995 In conclusion, the hydrophilic HMG-CoA reductase inhibitor fluvastatin at either 20 or 40 mg/day appears to be both safe and effective in lowering atherogenic lipids in renal transplant patients. Fluvastatin 59-70 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 31-48 7604797-1 1995 The long-term clinical efficacy of fluvastatin was assessed in 24 patients with familial hypercholesterolemia over a total treatment period of 104 weeks. Fluvastatin 35-46 low density lipoprotein receptor Homo sapiens 80-109 7604799-5 1995 Both drugs were equally effective in lowering LDL-C after 4 weeks of treatment (-24.0% with fluvastatin, -24.1% with pravastatin) but, after 16 weeks, LDL-C reduction was -30.4% with fluvastatin and -26.6% with pravastatin. Fluvastatin 183-194 component of oligomeric golgi complex 2 Homo sapiens 151-156 7604799-6 1995 This further lowering of LDL-C between week 4 and week 16 was significant (p < 0.001) for fluvastatin but not pravastatin. Fluvastatin 93-104 component of oligomeric golgi complex 2 Homo sapiens 25-30 7604802-0 1995 Changes in plasma apolipoprotein B-containing lipoparticle levels following therapy with fluvastatin and cholestyramine. Fluvastatin 89-100 apolipoprotein B Homo sapiens 18-34 7604802-3 1995 The effect on lipoparticle levels of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin, in combination with cholestyramine, was assessed in a double-blind randomized study. Fluvastatin 109-120 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 41-98 7604802-8 1995 Fluvastatin plus cholestyramine produced a significant (p < 0.001), dose-dependent reduction in levels of cholesterol (range, -29 to -34%), LDL-C (range, -30 to -44%), apo B (range, -23 to -34%), and apo E (range, -33 to -43%). Fluvastatin 0-11 apolipoprotein E Homo sapiens 203-208 7604809-6 1995 These effects on cholesterol levels were reflected in a significant decrease in apolipoprotein B levels with fluvastatin therapy (p < 0.001). Fluvastatin 109-120 apolipoprotein B Homo sapiens 80-96 7702230-10 1995 Fluvastatin, alone and combined with alcohol, resulted in similar decreases in levels of total cholesterol (22% and 23%, respectively; P < 0.001 when compared with baseline), low-density lipoprotein cholesterol (28% and 29%, respectively; P < 0.001 compared with baseline), and apolipoprotein B (17% and 20%, respectively; P < 0.001 compared with baseline). Fluvastatin 0-11 apolipoprotein B Homo sapiens 284-300 19496273-8 1994 Our group has studied the short- and long-term effect of fluvastatin on Lp(a) in hypercholesterolaemic patients; fluvastatin was found to have no effect in such patients as observed in the short-term studies, but significant reductions in Lp(a) levels were noted during long-term treatment. Fluvastatin 57-68 lipoprotein(a) Homo sapiens 72-77 7698284-0 1995 Inhibition of cholesterol synthesis ex vivo and in vivo by fluvastatin, a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. Fluvastatin 59-70 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 91-138 19496270-1 1994 Fluvastatin, a new synthetic inhibitor of HMGCoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, has been studied in several models to examine its effects when used in combination with other lipid-modifying agents such as derivatives of fibric acid (bezafibrate), resins (cholestyramine), and niacin. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 50-98 7979841-1 1994 BACKGROUND: Fluvastatin sodium is a new, entirely synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor that may be an effective lipid-lowering agent in patients whose hyperlipidemia does not respond to dietary therapy. Fluvastatin 12-30 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 60-107 7979841-8 1994 Fluvastatin sodium, the first totally synthetic 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor to be used in clinical trials, appears to be both effective and well tolerated at 20 mg/d, given in either a single or divided dose. Fluvastatin 0-18 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 48-95 7818592-3 1994 Fluvastatin sodium was administered to Watanabe heritable hyperlipidemic (WHHL) rabbits, a low density lipoprotein (LDL) receptor deficient animal model, for 6 weeks at doses of 12.5 mg/kg, 25 mg/kg, and 50 mg/kg. Fluvastatin 0-18 low-density lipoprotein receptor Oryctolagus cuniculus 91-129 8017464-3 1994 The effect of 6 weeks of treatment with fluvastatin (20 and 40 mg/day in the evening), a novel competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, on lipoparticle levels was studied in 423 patients with hypercholesterolemia after 14 weeks of standard dietary therapy. Fluvastatin 40-51 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 120-177 7958569-0 1994 Carcinogenicity and mutagenicity studies with fluvastatin, a new, entirely synthetic HMG-CoA reductase inhibitor. Fluvastatin 46-57 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 85-102 7974251-8 1994 These studies indicate that the adverse maternal effects observed with fluvastatin before or following parturition resulted from exaggerated pharmacologic activity at the dose levels administered, i.e., inhibition of the enzyme HMG-CoA reductase, its immediate product mevalonic acid, and cholesterol biosynthesis. Fluvastatin 71-82 3-hydroxy-3-methylglutaryl-CoA reductase Rattus norvegicus 228-245 8017467-4 1994 After 8 weeks of treatment, fluvastatin produced significant reductions from baseline of 17.4% (p < 0.001) in LDL-C, 13.2% (p < 0.001) in total cholesterol (TC), 13.8% (p < 0.001) in very low-density lipoprotein cholesterol (VLDL-C), and 6.4% (NS) in TG. Fluvastatin 28-39 component of oligomeric golgi complex 2 Homo sapiens 113-118 8017467-9 1994 At the end of the study, 43.8% of fluvastatin patients and 45% of gemfibrozil patients achieved a reduction of > 20% in LDL-C levels. Fluvastatin 34-45 component of oligomeric golgi complex 2 Homo sapiens 123-128 8017467-10 1994 Normalization of LDL-C levels was achieved (according to European Atherosclerosis Society guidelines) by 13.4% of fluvastatin- and 14.6% of gemfibrozil-treated patients. Fluvastatin 114-125 component of oligomeric golgi complex 2 Homo sapiens 17-22 8017468-6 1994 Fluvastatin significantly increased LpA-I (+8%) and apo E (+20%). Fluvastatin 0-11 apolipoprotein E Homo sapiens 52-57 8017468-12 1994 In conclusion, fluvastatin is a well tolerated 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor for the treatment of primary hypercholesterolemia. Fluvastatin 15-26 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 47-104 8017470-1 1994 The purpose of this study was to investigate the triglyceride-lowering effect of fluvastatin, a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, in the combined hyperlipidemia of non-insulin-dependent diabetes mellitus (NIDDM). Fluvastatin 81-92 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 100-157 8017471-4 1994 Thus, it is of interest to evaluate the efficacy, safety, and tolerability of the new lipid-lowering agent fluvastatin, a new, wholly synthetic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, in patients at high risk. Fluvastatin 107-118 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 144-201 8192170-0 1994 Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination. Fluvastatin 37-48 low density lipoprotein receptor Homo sapiens 75-104 8198018-1 1994 Fluvastatin sodium (Lescol; Sandoz) the first entirely synthetic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor studied, is structurally distinct from the other HMG-CoA reductase inhibitors currently available, all of which are fungal metabolites and analogues of compactin. Fluvastatin 0-18 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 65-122 8198018-1 1994 Fluvastatin sodium (Lescol; Sandoz) the first entirely synthetic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor studied, is structurally distinct from the other HMG-CoA reductase inhibitors currently available, all of which are fungal metabolites and analogues of compactin. Fluvastatin 20-26 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 65-122 8198023-3 1994 By weeks 9-12, fluvastatin decreased plasma LDL-C levels by 24.3% (p < 0.001) and plasma TG by 15.3% (p < 0.01). Fluvastatin 15-26 component of oligomeric golgi complex 2 Homo sapiens 44-49 8198023-6 1994 Fluvastatin is an effective treatment of combined elevations of TG and LDL-C in NIDDM. Fluvastatin 0-11 component of oligomeric golgi complex 2 Homo sapiens 71-76 7517835-1 1994 This multicentre open 6-week study evaluated the efficacy, safety and tolerability of fluvastatin, the first fully synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor, in elderly women with type IIa hypercholesterolaemia. Fluvastatin 86-97 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 125-182 7517835-7 1994 After 6 weeks, fluvastatin significantly (p < 0.001, ANOVA test) reduced total cholesterol, LDL cholesterol and apo B levels by 22%, 29% and 23%, respectively. Fluvastatin 15-26 apolipoprotein B Homo sapiens 115-120 7517836-12 1994 More women than men experienced a confirmed increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) when receiving fluvastatin. Fluvastatin 139-150 glutamic--pyruvic transaminase Homo sapiens 93-117 7517836-12 1994 More women than men experienced a confirmed increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) when receiving fluvastatin. Fluvastatin 139-150 solute carrier family 17 member 5 Homo sapiens 56-82 7517836-12 1994 More women than men experienced a confirmed increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) when receiving fluvastatin. Fluvastatin 139-150 solute carrier family 17 member 5 Homo sapiens 84-87 7986315-0 1994 Effect of fluvastatin on plasma apolipoprotein-B-containing particles, including lipoprotein(a). Fluvastatin 10-21 apolipoprotein B Homo sapiens 32-48 7986315-10 1994 Treatment with fluvastatin for 6 weeks was associated with a dose-dependent reduction of LDL cholesterol, apoB, LpE:B and LpCIII:B levels. Fluvastatin 15-26 apolipoprotein B Homo sapiens 106-110 8462179-5 1993 After 4 weeks of treatment with 40 mg of fluvastatin, the mean decrease in plasma LDL cholesterol (LDL-C) in patients with the genetically characterized "Sephardic" and "Lithuanian" mutations was 16-18%, whereas in the other three groups, it was 25-30% (p < 0.005). Fluvastatin 41-52 component of oligomeric golgi complex 2 Homo sapiens 82-97 7905274-3 1993 Thus, it is interesting to evaluate the efficacy, safety, and tolerability of the new lipid-lowering agent fluvastatin, a 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA)-reductase inhibitor, in patients receiving concomitant antihypertensive/cardiovascular drug treatments. Fluvastatin 107-118 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 122-180 7905274-8 1993 In patients taking fluvastatin and antihypertensives, confirmed (measured at two consecutive occasions) increases more than three times the upper limit of normal in aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) occurred in only two patients. Fluvastatin 19-30 glutamic--pyruvic transaminase Homo sapiens 203-227 7905274-8 1993 In patients taking fluvastatin and antihypertensives, confirmed (measured at two consecutive occasions) increases more than three times the upper limit of normal in aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) occurred in only two patients. Fluvastatin 19-30 glutamic--pyruvic transaminase Homo sapiens 229-233 8297542-3 1993 Thus, it is interesting to evaluate the efficacy and safety of fluvastatin, a new 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)-reductase inhibitor, in such a patient population. Fluvastatin 63-74 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 82-139 8345219-2 1993 Moreover, blockade of synthesis of these lipids with inhibitors of two of the rate-limiting enzymes, HMGCoA reductase (lovastatin, fluvastatin) and serine palmitoyl transferase (beta-chloroalanine), alters the kinetics of barrier repair. Fluvastatin 131-142 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 101-117 8466953-0 1993 Effect of fluvastatin sodium (XU62-320), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the induction of low-density lipoprotein receptor in HepG2 cells. Fluvastatin 10-28 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 60-107 8466953-0 1993 Effect of fluvastatin sodium (XU62-320), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the induction of low-density lipoprotein receptor in HepG2 cells. Fluvastatin 10-28 low density lipoprotein receptor Homo sapiens 129-161 8466953-0 1993 Effect of fluvastatin sodium (XU62-320), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the induction of low-density lipoprotein receptor in HepG2 cells. Fluvastatin 30-38 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 60-107 8466953-0 1993 Effect of fluvastatin sodium (XU62-320), a new inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on the induction of low-density lipoprotein receptor in HepG2 cells. Fluvastatin 30-38 low density lipoprotein receptor Homo sapiens 129-161 8466953-1 1993 The effect of fluvastatin sodium (XU62-320), a new type of inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, on the induction of LDL receptor in the human liver-derived cell line HepG2 was investigated. Fluvastatin 14-32 low density lipoprotein receptor Homo sapiens 131-143 8466953-1 1993 The effect of fluvastatin sodium (XU62-320), a new type of inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, on the induction of LDL receptor in the human liver-derived cell line HepG2 was investigated. Fluvastatin 34-42 low density lipoprotein receptor Homo sapiens 131-143 8466953-2 1993 Fluvastatin sodium produced marked inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and induction of LDL receptor on HepG2 cells at a concentration of 0.1-1.0 microM. Fluvastatin 0-18 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 49-96 8466953-2 1993 Fluvastatin sodium produced marked inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and induction of LDL receptor on HepG2 cells at a concentration of 0.1-1.0 microM. Fluvastatin 0-18 low density lipoprotein receptor Homo sapiens 123-135 8462179-5 1993 After 4 weeks of treatment with 40 mg of fluvastatin, the mean decrease in plasma LDL cholesterol (LDL-C) in patients with the genetically characterized "Sephardic" and "Lithuanian" mutations was 16-18%, whereas in the other three groups, it was 25-30% (p < 0.005). Fluvastatin 41-52 component of oligomeric golgi complex 2 Homo sapiens 99-104 8462180-4 1993 Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, is almost completely absorbed, actively targeted to the liver, and secreted in the bile. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 15-72 1600114-0 1992 Absorption and disposition of fluvastatin, an inhibitor of HMG-CoA reductase, in the rabbit. Fluvastatin 30-41 3-hydroxy-3-methylglutaryl-coenzyme A reductase Oryctolagus cuniculus 59-76 1640002-1 1992 The pharmacokinetics of fluvastatin, a potent inhibitor of hydroxymethylglutaryl-CoA reductase and thus cholesterol synthesis, have been studied in 24 normal male volunteers who received [3H] fluvastatin in three different studies: a single-dose study using oral doses of 2 or 10 mg, an absolute bioavailability study using doses of 2 mg intravenously or 10 mg orally, and a multiple-dose study using 40 mg orally once daily for 6 days. Fluvastatin 24-35 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 59-94 1569107-1 1992 Rat hepatic microsomal squalene synthetase (EC 2.5.1.21) was induced 25-fold by feeding rats with diet containing the hydroxymethylglutaryl-coenzyme A reductase inhibitor, fluvastatin, and cholestyramine, a bile acid sequestrant. Fluvastatin 172-183 farnesyl diphosphate farnesyl transferase 1 Rattus norvegicus 23-42 2207302-0 1990 Disposition of fluvastatin, an inhibitor of HMG-COA reductase, in mouse, rat, dog, and monkey. Fluvastatin 15-26 3-hydroxy-3-methylglutaryl-Coenzyme A reductase Mus musculus 44-61 1854361-0 1991 Effects of fluvastatin (XU 62-320), an HMG-CoA reductase inhibitor, on the distribution and composition of low density lipoprotein subspecies in humans. Fluvastatin 11-22 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 39-56 1854361-1 1991 We studied the effect of fluvastatin (XU 62-320), a new HMG-CoA reductase inhibitor, on the distribution of low density lipoprotein (LDL) subspecies and composition in humans. Fluvastatin 25-36 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 56-73 1854361-6 1991 However, the LDL-cholesterol/apo B ratio changes were relatively small in all fluvastatin-treated individuals including the group with changes in electrophoretic mobility, confirming that HMG-CoA reductase inhibitor causes relatively small and subtle changes in the distribution of LDL subspecies. Fluvastatin 78-89 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 188-205 33793833-0 2021 Fluvastatin protects neuronal cells from hydrogen peroxide-induced toxicity with decreasing oxidative damage and increasing PI3K/Akt/mTOR signalling. Fluvastatin 0-11 AKT serine/threonine kinase 1 Homo sapiens 129-132 2361135-1 1990 The mechanism of slow binding inhibition of 3-hydroxy-3-methylglutaryl- coenzyme A reductase by lovastatin, fluindostatin, and related compounds was studied. Fluvastatin 108-121 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 44-92 33793833-0 2021 Fluvastatin protects neuronal cells from hydrogen peroxide-induced toxicity with decreasing oxidative damage and increasing PI3K/Akt/mTOR signalling. Fluvastatin 0-11 mechanistic target of rapamycin kinase Homo sapiens 133-137 33793833-8 2021 In contrast, PI3K/Akt/mTOR activation mediated fluvastatin"s neuroprotective activity (P < 0.05). Fluvastatin 47-58 AKT serine/threonine kinase 1 Homo sapiens 18-21 33793833-8 2021 In contrast, PI3K/Akt/mTOR activation mediated fluvastatin"s neuroprotective activity (P < 0.05). Fluvastatin 47-58 mechanistic target of rapamycin kinase Homo sapiens 22-26 33793833-9 2021 CONCLUSIONS: Our work demonstrates the beneficial effects of fluvastatin in neuronal cells under pathological conditions, and, furthermore, this is via prenylation-independent activation of PI3K/Akt/mTOR pathway. Fluvastatin 61-72 AKT serine/threonine kinase 1 Homo sapiens 195-198 33793833-9 2021 CONCLUSIONS: Our work demonstrates the beneficial effects of fluvastatin in neuronal cells under pathological conditions, and, furthermore, this is via prenylation-independent activation of PI3K/Akt/mTOR pathway. Fluvastatin 61-72 mechanistic target of rapamycin kinase Homo sapiens 199-203 15557765-8 2004 In a subgroup of patients with CRP, IL-6, sIL-6R, and ox-LDL baseline serum values > or = the median and IL-10 < or = the median, CRP was reduced on day 28 of fluvastatin treatment (p < 0.01), IL-6 and ox-LDL were reduced earlier, on day 14 (p = 0.05 and p < 0.05, respectively) while sIL-6R did not change significantly during the treatment period. Fluvastatin 165-176 C-reactive protein Homo sapiens 136-139 34826718-1 2022 This article reports the interaction between a synthetic statin, fluvastatin with bovine milk protein, beta-lactoglobulin (BLG) through docking, constant pH molecular dynamics simulation (cpHMD) and binding free energy calculations. Fluvastatin 65-76 casein beta Bos taurus 89-101 34826718-1 2022 This article reports the interaction between a synthetic statin, fluvastatin with bovine milk protein, beta-lactoglobulin (BLG) through docking, constant pH molecular dynamics simulation (cpHMD) and binding free energy calculations. Fluvastatin 65-76 beta-lactoglobulin Bos taurus 103-121 34826718-1 2022 This article reports the interaction between a synthetic statin, fluvastatin with bovine milk protein, beta-lactoglobulin (BLG) through docking, constant pH molecular dynamics simulation (cpHMD) and binding free energy calculations. Fluvastatin 65-76 beta-lactoglobulin Bos taurus 123-126 34826718-13 2022 This study suggests that in spite of the acidic environment in the stomach BLG can act as a carrier for the acid-sensitive drug molecules such as fluvastatin because of its highly stable conformational behavior in the acidic pH. Fluvastatin 146-157 beta-lactoglobulin Bos taurus 75-78 34883342-0 2022 Fluvastatin enhances IL-33-mediated mast cell IL-6 and TNF production. Fluvastatin 0-11 interleukin 33 Homo sapiens 21-26 34883342-0 2022 Fluvastatin enhances IL-33-mediated mast cell IL-6 and TNF production. Fluvastatin 0-11 interleukin 6 Homo sapiens 46-50 34883342-0 2022 Fluvastatin enhances IL-33-mediated mast cell IL-6 and TNF production. Fluvastatin 0-11 tumor necrosis factor Homo sapiens 55-58 34883342-5 2022 In contrast to IgE signaling, we show that fluvastatin augments IL-33-induced TNF and IL-6 production by mast cells. Fluvastatin 43-54 tumor necrosis factor Homo sapiens 78-81 34883342-5 2022 In contrast to IgE signaling, we show that fluvastatin augments IL-33-induced TNF and IL-6 production by mast cells. Fluvastatin 43-54 interleukin 6 Homo sapiens 86-90 34883342-7 2022 Treatment of IL-33-activated mast cells with mevalonic acid or isoprenoids reduced fluvastatin effects, suggesting fluvastatin acts at least partly by reducing isoprenoid production. Fluvastatin 83-94 interleukin 33 Homo sapiens 13-18 34883342-7 2022 Treatment of IL-33-activated mast cells with mevalonic acid or isoprenoids reduced fluvastatin effects, suggesting fluvastatin acts at least partly by reducing isoprenoid production. Fluvastatin 115-126 interleukin 33 Homo sapiens 13-18 34883342-8 2022 Fluvastatin also enhanced IL-33-induced NF-kappaB transcriptional activity and promoted neutrophilic peritonitis in vivo, a response requiring mast cell activation. Fluvastatin 0-11 interleukin 33 Homo sapiens 26-31 34883342-8 2022 Fluvastatin also enhanced IL-33-induced NF-kappaB transcriptional activity and promoted neutrophilic peritonitis in vivo, a response requiring mast cell activation. Fluvastatin 0-11 nuclear factor kappa B subunit 1 Homo sapiens 40-49 34927546-0 2021 Fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6). Fluvastatin 0-11 sirtuin 6 Homo sapiens 137-146 34927546-9 2021 To sum up, this study firstly evidenced that fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by regulating SIRT6 expression. Fluvastatin 45-56 sirtuin 6 Homo sapiens 180-185 34927546-0 2021 Fluvastatin suppresses the proliferation, invasion, and migration and promotes the apoptosis of endometrial cancer cells by upregulating Sirtuin 6 (SIRT6). Fluvastatin 0-11 sirtuin 6 Homo sapiens 148-153 34927546-1 2021 Fluvastatin, the first fully synthesized 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR) inhibitor, has been reported to inhibit the development and metastasis of multiple cancers. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 41-98 34927546-1 2021 Fluvastatin, the first fully synthesized 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (HMGCR) inhibitor, has been reported to inhibit the development and metastasis of multiple cancers. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 100-105 34927546-7 2021 The expression of SIRT6 was elevated in EC cells upon fluvastatin exposure. Fluvastatin 54-65 sirtuin 6 Homo sapiens 18-23 34927546-8 2021 After silencing SIRT6 in fluvastatin-treated EC cells, the proliferation, migration, and invasion were promoted whereas the apoptosis was decreased. Fluvastatin 25-36 sirtuin 6 Homo sapiens 16-21 34773069-0 2022 Fluvastatin sensitizes pancreatic cancer cells toward radiation therapy and suppresses radiation- and/or TGF-beta-induced tumor-associated fibrosis. Fluvastatin 0-11 transforming growth factor alpha Mus musculus 105-113 34761894-5 2021 In addition, released fluvastatin sodium (Flu) by the NPs acted on monocarboxylic acid transporter 4 (MCT4) in the cell membrane to inhibit lactate leakage and induce a decrease of intracellular pH, further prompting the NPs to release chlorine dioxide (ClO2), which then oxidized methionine, inhibited tumor growth, and produced large numbers of Cl- in the cytoplasm. Fluvastatin 22-40 solute carrier family 16 member 4 Homo sapiens 67-100 34761894-5 2021 In addition, released fluvastatin sodium (Flu) by the NPs acted on monocarboxylic acid transporter 4 (MCT4) in the cell membrane to inhibit lactate leakage and induce a decrease of intracellular pH, further prompting the NPs to release chlorine dioxide (ClO2), which then oxidized methionine, inhibited tumor growth, and produced large numbers of Cl- in the cytoplasm. Fluvastatin 22-40 solute carrier family 16 member 4 Homo sapiens 102-106 34761894-5 2021 In addition, released fluvastatin sodium (Flu) by the NPs acted on monocarboxylic acid transporter 4 (MCT4) in the cell membrane to inhibit lactate leakage and induce a decrease of intracellular pH, further prompting the NPs to release chlorine dioxide (ClO2), which then oxidized methionine, inhibited tumor growth, and produced large numbers of Cl- in the cytoplasm. Fluvastatin 42-45 solute carrier family 16 member 4 Homo sapiens 67-100 34761894-5 2021 In addition, released fluvastatin sodium (Flu) by the NPs acted on monocarboxylic acid transporter 4 (MCT4) in the cell membrane to inhibit lactate leakage and induce a decrease of intracellular pH, further prompting the NPs to release chlorine dioxide (ClO2), which then oxidized methionine, inhibited tumor growth, and produced large numbers of Cl- in the cytoplasm. Fluvastatin 42-45 solute carrier family 16 member 4 Homo sapiens 102-106 34773069-9 2022 Interestingly, fluvastatin suppressed radiation and/or TGF-beta-induced activation of PSCs, as well as the fibrogenic properties of these cells in vitro. Fluvastatin 15-26 transforming growth factor alpha Mus musculus 55-63 34594412-0 2021 Novel function of fluvastatin in attenuating oxidized low-density lipoprotein-induced endothelial cell ferroptosis in a glutathione peroxidase4- and cystine-glutamate antiporter-dependent manner. Fluvastatin 18-29 glutathione peroxidase 4 Homo sapiens 120-143 34858338-13 2021 The Matsuda index, as an indicator of insulin sensitivity, was lower after fluvastatin intake, but the difference was not statistically significant (p=0.09). Fluvastatin 75-86 insulin Homo sapiens 38-45 34649351-4 2021 Notably, the elevated levels of DAF and NF-kB expression persisted following treatment with fluvastatin. Fluvastatin 92-103 CD55 molecule (Cromer blood group) Homo sapiens 32-35 34594412-11 2021 Furthermore, knockdown of GPx4 and xCT expression blunted the protective effects of fluvastatin on ox-LDL-treated endothelial cells. Fluvastatin 84-95 glutathione peroxidase 4 Homo sapiens 26-30 35209778-2 2022 Fluvastatin (FV) is a fully synthetic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor used as a cholesterol-lowering agent in patients with hypercholesterolemia. Fluvastatin 0-11 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-91 34594412-11 2021 Furthermore, knockdown of GPx4 and xCT expression blunted the protective effects of fluvastatin on ox-LDL-treated endothelial cells. Fluvastatin 84-95 solute carrier family 7 member 11 Homo sapiens 35-38 34594412-12 2021 These data indicated a novel function of fluvastatin in the protection of endothelial cells from ox-LDL-induced ferroptosis, the mechanism of which involves the regulation of GPx4 and xCT. Fluvastatin 41-52 glutathione peroxidase 4 Homo sapiens 175-179 34594412-12 2021 These data indicated a novel function of fluvastatin in the protection of endothelial cells from ox-LDL-induced ferroptosis, the mechanism of which involves the regulation of GPx4 and xCT. Fluvastatin 41-52 solute carrier family 7 member 11 Homo sapiens 184-187 34762363-5 2021 Biotinylation assays showed that acute (1hr) atorvastatin, simvastatin, or fluvastatin increased AQP2 membrane accumulation in mCCDc1l cells showing that the cell line responds to acute statin treatment. Fluvastatin 75-86 aquaporin 2 Mus musculus 97-101 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Fluvastatin 125-136 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 33-65 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Fluvastatin 125-136 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 67-71 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Fluvastatin 125-136 ATP binding cassette subfamily B member 1 Homo sapiens 77-91 34162690-5 2021 In our study, apically expressed breast cancer resistance protein (BCRP) and P-glycoprotein (P-gp) transported atorvastatin, fluvastatin, pitavastatin, and rosuvastatin. Fluvastatin 125-136 ATP binding cassette subfamily B member 1 Homo sapiens 93-97 34162690-6 2021 Multidrug resistance-associated protein 3 (MRP3) transported atorvastatin, fluvastatin, pitavastatin, and to a smaller extent, pravastatin. Fluvastatin 75-86 ATP binding cassette subfamily C member 3 Homo sapiens 0-41 34162690-6 2021 Multidrug resistance-associated protein 3 (MRP3) transported atorvastatin, fluvastatin, pitavastatin, and to a smaller extent, pravastatin. Fluvastatin 75-86 ATP binding cassette subfamily C member 3 Homo sapiens 43-47 34162690-7 2021 MRP4 transported fluvastatin and rosuvastatin. Fluvastatin 17-28 ATP binding cassette subfamily C member 4 Homo sapiens 0-4 34162690-10 2021 MRP3, on the other hand, may contribute to 33-38% and 35-51% of total active efflux of atorvastatin, fluvastatin, and pitavastatin in jejunal enterocytes and liver hepatocytes, respectively. Fluvastatin 101-112 ATP binding cassette subfamily C member 3 Homo sapiens 0-4 35575209-3 2022 To address these issues, an inhalable nanoreactor was proposed by spontaneously adsorbing biomimetic protein corona (PC) composed of matrix metalloproteinase 2 responsive gelatin and glutamate (Glu) on the surface of cationic nanostructured lipid carriers (NLC) core loaded with ferrocene (Fc) and fluvastatin. Fluvastatin 298-309 matrix metallopeptidase 2 Homo sapiens 133-159 35575209-5 2022 Mechanically, fluvastatin was proved to inhibit monocarboxylic acid transporter 4 mediated lactate efflux, inducing tumor acidosis to boost Fc-catalyzing reactive oxygen species production, while the extracellular elevating Glu concentration was found to inhibit xCT (system Xc-) functions and further collapse the tumor antioxidant system by glutathione synthesis suppression. Fluvastatin 14-25 solute carrier family 7 member 11 Homo sapiens 263-266 35563736-0 2022 Expression of Caspase-3 in Circulating Innate Lymphoid Cells Subtypes Is Altered by Treatment with Metformin and Fluvastatin in High-Fat Diet Fed C57BL/6 Mice. Fluvastatin 113-124 caspase 3 Mus musculus 14-23 35563736-2 2022 Another critical point was to assess the therapeutic effects of metformin and fluvastatin in modulating caspase-3 activation in ILCs within these HFD-fed mice. Fluvastatin 78-89 caspase 3 Mus musculus 104-113 35563736-5 2022 Notably, six-week treatment with metformin and fluvastatin reduced the caspase-3 activation in ILC subtypes. Fluvastatin 47-58 caspase 3 Mus musculus 71-80 35563736-7 2022 Interestingly, the reduced caspase-3 activation in ILC3 was associated with lower total cholesterol following fluvastatin treatment in these HFD-fed mice. Fluvastatin 110-121 caspase 3 Mus musculus 27-36 35422113-4 2022 We observed that fluvastatin and pitavastatin showed fair, binding affinities to RNA polymerase and 3-CL-Pro, whereas fluvastatin showed the strongest binding affinity to the helicase. Fluvastatin 118-129 helicase for meiosis 1 Homo sapiens 175-183 35422113-5 2022 Fluvastatin also showed the highest affinity for the SpikeDelta and a fair docking score for other spike variants. Fluvastatin 0-11 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 99-104 35422113-7 2022 Thus our study shows that of all the statins, fluvastatin can bind to multiple target proteins of SARS-CoV-2, including the spike-mutant proteins. Fluvastatin 46-57 surface glycoprotein Severe acute respiratory syndrome coronavirus 2 124-129 34230964-7 2021 Remarkably, lipid-lowering fluvastatin improves respiratory anomalies in Mecp2-mutant mice. Fluvastatin 27-38 methyl CpG binding protein 2 Mus musculus 73-78 34721731-15 2021 Combining CTRP and CMap analyses, fluvastatin was identified as a promising therapeutic agent against HCC. Fluvastatin 34-45 cystatin F Homo sapiens 19-23 34572136-4 2021 Four statins, namely simvastatin, atorvastatin, lovastatin, and fluvastatin, decreased PD-L1 expression in melanoma and lung cancer cells. Fluvastatin 64-75 CD274 molecule Homo sapiens 87-92 34162690-14 2021 Significance Statement This study characterized and compared the transport of atorvastatin, fluvastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin acid, and four atorvastatin metabolites by six ABC transporters (BCRP, MRP2, MRP3, MRP4, MRP8, P-gp). Fluvastatin 92-103 ATP binding cassette subfamily B member 6 (Langereis blood group) Homo sapiens 209-212 34452303-3 2021 The synthesis of orbivirus outer-capsid protein VP2 (detected by confocal immunofluorescence imaging) was used to assess levels of virus replication, showing a reduction in fluvastatin-treated cells. Fluvastatin 173-184 VP2 Bluetongue virus 48-51 34452303-6 2021 Fluvastatin, which inhibits 3-hydroxy 3-methyl glutaryl CoA reductase in the mevalonic acid pathway, disrupts these NS4 interactions. Fluvastatin 0-11 SOS Ras/Rac guanine nucleotide exchange factor 1 Homo sapiens 116-119 34452303-9 2021 Pre-treatment of IFNAR(-/-) mice with fluvastatin promoted their survival upon challenge with live BTV, although only limited protection was observed. Fluvastatin 38-49 interferon (alpha and beta) receptor 1 Mus musculus 17-22 35209778-2 2022 Fluvastatin (FV) is a fully synthetic hydroxymethyl glutaryl coenzyme A (HMG-CoA) reductase inhibitor used as a cholesterol-lowering agent in patients with hypercholesterolemia. Fluvastatin 13-15 3-hydroxy-3-methylglutaryl-CoA reductase Homo sapiens 38-91 35465754-0 2022 Targeting p-AKT/mTOR/MAP kinase signaling, NLRP3 inflammasome and apoptosis by fluvastatin with or without taxifolin mitigates gonadal dysfunction induced by bisphenol-A in male rats. Fluvastatin 79-90 AKT serine/threonine kinase 1 Rattus norvegicus 12-15 34853441-0 2022 Correction to: Fluvastatin sensitizes pancreatic cancer cells toward radiation therapy and suppresses radiation- and/or TGF-beta-induced tumor-associated fibrosis. Fluvastatin 15-26 transforming growth factor alpha Homo sapiens 120-128 35465754-0 2022 Targeting p-AKT/mTOR/MAP kinase signaling, NLRP3 inflammasome and apoptosis by fluvastatin with or without taxifolin mitigates gonadal dysfunction induced by bisphenol-A in male rats. Fluvastatin 79-90 mechanistic target of rapamycin kinase Rattus norvegicus 16-20 35465754-0 2022 Targeting p-AKT/mTOR/MAP kinase signaling, NLRP3 inflammasome and apoptosis by fluvastatin with or without taxifolin mitigates gonadal dysfunction induced by bisphenol-A in male rats. Fluvastatin 79-90 NLR family, pyrin domain containing 3 Rattus norvegicus 43-48