Nystatin (Sigma-Aldrich, Taufkirchen, Germany), fluconazole (Sigma-Aldrich, Taufkirchen, Germany) and atorvastatin (Sigma-Aldrich, Taufkirchen, Germany) were tested against all the strains. To prepare stock solutions of each drug, fluconazole and atorvastatin were diluted with dimethyl sulfoxide (DMSO) (Merck, Darmstadt, Hesse, Germany), and Nystatin was dissolved in methanol. Stock solutions were stored at −20°C.
Atorvastatin
Manufactured by Merck Group
Sourced in United States, Germany, United Kingdom, China
Atorvastatin is a laboratory equipment product manufactured by Merck Group. It is a type of statin, a class of medications used to lower cholesterol levels. The core function of Atorvastatin is to inhibit the enzyme HMG-CoA reductase, which plays a crucial role in the production of cholesterol in the body.
Automatically generated - may contain errors
Lab products found in correlation
Simvastatin, by Merck Group (28 mentions)
Rosuvastatin, by Merck Group (14 mentions)
Lovastatin, by Merck Group (12 mentions)
Fluvastatin, by Merck Group (11 mentions)
Fetal bovine serum (fbs), by Thermo Fisher Scientific (11 mentions)
Dimethyl sulfoxide (dmso), by Merck Group (10 mentions)
Pravastatin, by Merck Group (10 mentions)
Cholesterol, by Merck Group (6 mentions)
Mevalonate, by Merck Group (6 mentions)
Metformin, by Merck Group (5 mentions)
Nystatin, by Merck Group (4 mentions)
Fluconazole, by Merck Group (4 mentions)
Mevastatin, by Merck Group (4 mentions)
Quercetin, by Merck Group (4 mentions)
Losartan, by Merck Group (3 mentions)
Enalapril, by Merck Group (3 mentions)
Ammonium acetate, by Merck Group (3 mentions)
Fti 277, by Merck Group (3 mentions)
Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (3 mentions)
Bovine serum albumin (bsa), by Merck Group (3 mentions)
142 protocols using atorvastatin
1
Antifungal and Antihyperlipidemic Drug Assay
2
Solubilization of Pharmaceutical Compounds
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
Lithium, atorvastatin, fluvastatin, and simvastatin were purchased from Sigma‐Aldrich. atorvastatin was also purchased from Merck Life Science (prevention and potassium‐deficient [KD] animal experiment). The atorvastatin was dissolved in dimethyl sulfoxide forming a 10 mg/ml stock solution. simvastatin, which is a prodrug, was diluted in ethanol followed by activation in NaOH and then heating for 2 h at 50°C. The solution was neutralized with HCl and adjusted with phosphate buffered saline (PBS) to a stock solution of 10 mg/ml.
3
Modulation of BMDC function by Ang2 and Atorvastatin
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
Bone marrow-derived dendritic cells (BMDCs) obtained from approximately 6-week-old C57BL/6 mice were cultured in RPMI 1640 media supplemented with 10 ng/mL granulocyte-macrophage colony-stimulating factor (GM-CSF) and 1 ng/mL IL-4 at 37°C in 5% humidified CO2 for 4 h. Medium containing nonadherent cells was replaced with fresh medium every 2 days. On culture day 7, the cells were treated with either Ang 2 (100 nM) (Sigma-Aldrich, St. Louis, MO, USA) alone or in combination with various concentrations (2.5, 5, or 10 μM) of atorvastatin (Sigma-Aldrich, St. Louis, MO, USA) for 24 h. Phosphate-buffered saline (PBS) was used as a control. In the inhibitor experiment, cells were exposed to Ang 2 (100 nM) for 24 h after pretreatment with an inhibitor (LY294002, 100 nM) for 1 h, whereas in the Nrf 2 activator experiment, cells were exposed to Ang 2 (100 nM) for 24 h after pretreatment with either 10 μM atorvastatin or 10 μM sulforaphane (SUL, Sigma-Aldrich, St. Louis, MO, USA) for 1 h. The antibodies for Akt, phospho-Akt (Ser473), and Nrf 2 (Ser40), as well as the inhibitor LY294002, were purchased from Cell Signaling Technology (Beverly, MA, USA).
4
Modulation of PBMC activation by atorvastatin and lipid metabolites
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
2.5 × 105 PBMCs per well were plated in a 96 U-bottomed plate and stimulated with 100ng/ml SEB (Sigma) or soluble α-CD3 (1.5μg/ml) and α-CD28 (0.5μg/ml; BD Biosciences) for 24, 48 or 72 hrs at 37°C, 5% CO2 in the presence or absence of atorvastatin (0.5 μg/ml, 1 μg/ml or 2 μg/ml; Sigma-Aldrich). For some experiments PBMCs were stimulated in the presence of cholesterol (50μM, 100μM and 200μM; Sigma-Aldrich), L-mevalonate (lithium salt, 100μM; Sigma-Aldrich), farnesyl (5μM, Sigma-Aldrich) or rapamycin (25nM, 50nM and 100nM; Sigma-Aldrich) with atorvastatin. Unstimulated and untreated PBMCs were used as negative controls.
5
Mevalonate Pathway Reverses Atorvastatin-Sensitive Phenotype
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
To determine if metabolic intermediates of the mevalonate pathway or LDL treatment revert the cells’ atorvastatin-sensitive phenotype, the statin-sensitive cancer cell line HOP-92 was seeded in 12-well plates at a density of 1 × 105 cells/mL (1 mL/well), incubated overnight, and then treated with 10 μM atorvastatin and various concentrations of R-mevalonic acid (10–50 μM; Sigma-Aldrich, St. Louis, MO), ubiquinone (25–200 μM; Wako, Osaka, Japan), dolichol (75–300 μM; Avanti Polar Lipids, Alabaster, AL), squalene (10–100 μM; Wako), FPP (1–25 μM; Echelon, Salt Lake City, UT), GGPP (1–25 μM; Sigma-Aldrich), or LDL (50–200 μg/mL; Alfa Aesar, Ward Hill, MA) for 48 hours. We chose the doses of each substrate according to published references [53 (link), 54 (link)]. In select experiments, we photographed these cells with a phase-contrast microscope to capture any morphological changes. After the incubation, cells were harvested, and cell numbers were counted using a Scepter handheld automated cell counter (Millipore). Statistical analyses were performed using one-way ANOVA and Bonferroni-Dunn post-hoc tests. P values of less than 0.05 were considered statistically significant.
6
Mevalonic Acid Reverses Atorvastatin Effects
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
To determine whether mevalonic acid treatment reverted the atorvastatin-sensitive phenotype, the cell lines whose proliferation was inhibited by atorvastatin were seeded in 6-well plates at a density of 1 × 105 cells/ml, incubated overnight, and then treated with 10 µM atorvastatin and various concentrations (25 µM, 50 µM, 100 µM, and 200 µM) of R-mevalonic acid (Sigma-Aldrich) for 24 hours. These cells were also photographed with a phase-contrast microscope to capture any morphological changes.
7
Endothelial Cell Response to Hypoxia and Atorvastatin
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
HUVECs (BD Biosciences) were cultured in EC medium with 2% endotoxin-free heat-inactivated fetal bovine serum (FBS; Life Technologies) until they reached the required confluence for each experiment. During 8 hours of normoxia, IH, or continuous hypoxia, HUVECs were incubated with either 20% normal human serum or heat-inactivated serum (Sigma-Aldrich) as detailed for each experiment. For atorvastatin experiments, HUVECs were incubated with 20% normal serum with or without addition of 1 μM atorvastatin (Sigma-Aldrich) for 8 hours in normoxia, IH, or continuous hypoxia. Passages 3 to 5 were used for all experiments. HEK293 [American Type Culture Collection (ATCC)] were cultured in Eagle's minimum essential medium with 10% FBS (ATCC).
8
Modulation of Trypanosoma cruzi Infection
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
Depending on the experiment, PMA-induced U937 cells were treated with drugs and inhibitors before incubation with T. cruzi trypomastigotes. 0.1 to 10 µM Atorvastatin (Sigma-Aldrich, USA) was incubated for 24 h, 10 µM of the ROCK inhibitor Y-27632 (Cell Signaling, USA), 10 µM of the p65 nuclear translocation inhibitor JSH-23 (Sigma-Aldrich, USA), and 1 µM of the TLR4 inhibitor TAK-242 (Sigma-Aldrich, USA) were incubated for 1 h. Dimethyl sulfoxide (DMSO) was used as a solvent at 0.1%. 1 µg/mL of the RhoA inhibitor C3 exoenzyme (26 (link)) (Cytoskeleton, USA) was incubated for 24 h, and C3 buffer (500 mM Imidazole, 50 mM Tris HCl, 1 mM MgCl2, 200 mM NaCl, 5% sucrose and 1% dextran) was used as a vehicle. 10 µM Geranylgeranyl pyrophosphate ammonium salt (GGPP) (Sigma-Aldrich, USA) was used to study the reversion of Atorvastatin inhibition of RhoA prenylation.
9
Endothelial Cell Response to Hypoxia and Atorvastatin
10
Evaluation of Cardiovascular Biomarkers
Check if the same lab product or an alternative is used in the 5 most similar protocols
+ Expand
Losartan, aspirin, and atorvastatin were purchased from Merck Sharp & Dohme Co., Ltd. (Cramlington, UK), Bayer Healthcare (Beijing, China) Co., Ltd. (Beijing, China), and Pfizer Pharmaceutical Co., Ltd. (New York, NY, USA), respectively. Ang II, renin, ET-1, IL-6, and NE ELISA kits were obtained from Cusabio Technology Co., Ltd. (Wuhan, China). ALD ELISA kits were obtained from Shanghai Enzyme-linked Biotechnology Co., Ltd. (Shanghai, China).
About PubCompare
Our mission is to provide scientists with the largest repository of trustworthy protocols and intelligent analytical tools, thereby offering them extensive information to design robust protocols aimed at minimizing the risk of failures.
We believe that the most crucial aspect is to grant scientists access to a wide range of reliable sources and new useful tools that surpass human capabilities.
However, we trust in allowing scientists to determine how to construct their own protocols based on this information, as they are the experts in their field.
Ready to get started?
Sign up for free.
Registration takes 20 seconds.
Available from any computer
No download required
Revolutionizing how scientists
search and build protocols!