Brl37344

Manufactured by Merck Group

Sourced in United States

BRL37344 is a laboratory equipment product from Merck Group. It is a synthetic compound primarily used in research and development applications. The core function of BRL37344 is to serve as a reference standard or analytical tool for various experimental procedures. Further details about its intended use or applications are not available.

Automatically generated - may contain errors

Lab products found in correlation

Alzet osmotic pump, by Durect (3 mentions) Clenbuterol, by Merck Group (3 mentions) Isoproterenol, by Merck Group (3 mentions) Phosphate buffered saline (pbs), by Thermo Fisher Scientific (2 mentions) Alzet pumps, by Thermo Fisher Scientific (2 mentions) Norepinephrine, by Merck Group (2 mentions) Low adhesion tissue culture plates, by STEMCELL (2 mentions) Euthyrox, by Merck Group (1 mentions) Lipofectamine 3000, by Thermo Fisher Scientific (1 mentions) Neutrophil elastase, by Abcam (1 mentions) Sr59230a, by Merck Group (1 mentions) Ifn γ, by Abcam (1 mentions) Adrb3, by Abcam (1 mentions) Fibrillarin, by Abcam (1 mentions) Pd l1, by Abcam (1 mentions) Indomethacin, by Abcam (1 mentions) Tyramine, by Merck Group (1 mentions) Sr59230a, by Santa Cruz Biotechnology (1 mentions) Superscript 3 reverse transcriptase, by Thermo Fisher Scientific (1 mentions) Nupage gel, by Thermo Fisher Scientific (1 mentions)

21 protocols using brl37344

Hypoxia-Induced Pulmonary Artery Smooth Muscle Cell Proliferation

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Human pulmonary artery smooth muscle cells were purchased from ScienCell Research Laboratories (Carlsbad, CA, US) and cultured in a specific medium (Sciencell No. 1101, Carlsbad, CA, US) supplemented with 2 % fetal bovine serum 100 U/mL penicillin, 100 µg/mL streptomycin, and 1 % smooth muscle cells growth supplement (Sciencell No. 1152, Carlsbad, CA, USA) in a humidified incubator with a constant supply of 5 % CO₂ at 37 °C to be used for experiments at passages 3–7.
Human pulmonary artery smooth muscle cells were seeded in gelatin 0.1 % coated 48-well plates (same number per well) and starved in medium with 0.4 % FBS for 24 h and then incubated under either normoxic or hypoxic (3 % O₂, 5 % CO₂ at 37 °C) conditions for 72 h. For treatment, cells were co-incubated with BRL37344 (0.001 μM) alone or associated with NG-nitro-l-arginine methyl ester (L-NAME 10 mM, Sigma-Aldrich Co. LLC.) during the hypoxia exposure. Human pulmonary artery smooth muscle cells proliferation was determined by cell counting using flow cytometry. All experiments were performed in triplicate.

García-Álvarez A., Pereda D., García-Lunar I., Sanz-Rosa D., Fernández-Jiménez R., García-Prieto J., Nuño-Ayala M., Sierra F., Santiago E., Sandoval E., Campelos P., Agüero J., Pizarro G., Peinado V.I., Fernández-Friera L., García-Ruiz J.M., Barberá J.A., Castellá M., Sabaté M., Fuster V, & Ibañez B. (2016). Beta-3 adrenergic agonists reduce pulmonary vascular resistance and improve right ventricular performance in a porcine model of chronic pulmonary hypertension. Basic Research in Cardiology, 111, 49.

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Intraperitoneal BRL37344 and Levothyroxine in Obese and DM Mice

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To activate the BAT, eight obese mice, six DM mice, and six control mice received intraperitoneal injection of BRL37344 (4-[-[[2-hydroxy-[3-chlorophenyl] ethyl]-amino] propyl] phenoxyacetate, Sigma Aldrich Inc., St. Louis, MO, USA) at 2.5 mg/kg three times per week for two weeks, whereas six obese mice, five DM mice, and six control mice received levothyroxine (Euthyrox, Merck KGaA, Germany) intervention at 30 µg/kg via intragastric administration three times per week for two weeks (Table 1). A total of nine normal mice that received no treatment were served as controls. The obese and DM mice were maintained on the high-fat diet during the whole experiment.

Wu C., Cheng W., Sun Y., Dang Y., Gong F., Zhu H., Li N., Li F, & Zhu Z. (2014). Activating Brown Adipose Tissue for Weight Loss and Lowering of Blood Glucose Levels: A MicroPET Study Using Obese and Diabetic Model Mice. PLoS ONE, 9(12), e113742.

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Characterization of ADRB3 Signaling Pathway

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β3-adrenoceptor agonist BRL 37344, antagonist SR59230A were from Sigma-Aldrich (St. Louis, MO). mTOR, p-CENP-A (S7), p-Rb (S780), Cyclin D1, p-Rictor (T1135), p-4E-BP1(T37/46), p-AKT (S473), p53, flag, PML, and Ki-67 antibody were from Cell Signaling (Danvers, MA). ADRB3, MPO, interleukin-6 (IL-6), Nucleolin, Fibrillarin, Neutrophil elastase (NE), IFN-γ, PD-L1, CD8, and CD68 antibody were from Abcam (Cambridge, MA). Transfections were performed using Lipofectamine 3000 (Invitrogen) for plasmid. The pcDNA3-Flag-ADRB3 was constructed by our lab.

Zhou Z., Zhan J., Luo Q., Hou X., Wang S., Xiao D., Xie Z., Liang H., Lin S, & Zheng M. (2022). ADRB3 induces mobilization and inhibits differentiation of both breast cancer cells and myeloid-derived suppressor cells. Cell Death & Disease, 13(2), 141.

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Preparation of Vasoconstrictive Agents

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Carbachol, methoctramine, and BRL-37344 (Sigma Aldrich), indomethacin (Abcam), denopamine (Santa Cruz), and α,β-methylene ATP (Cayman) were dissolved in DMSO, ethanol, or distilled water as appropriate. Krebs solution was composed of: (m m) 120 NaCl, 5.9 KCl, 25 NaHCO₃, 1.2 NaH₂PO₄·2H₂O, 5.5 glucose, 1.2 MgCl₂, and 2.5 CaCl₂. pH was adjusted to 7.4 by bubbling the solution with 95% O₂,−5% CO₂.

Alkawadri T., Wong P.Y., Fong Z., Lundy F.T., McGarvey L.P., Hollywood M.A., Thornbury K.D, & Sergeant G.P. (2022). M2 Muscarinic Receptor-Dependent Contractions of Airway Smooth Muscle are Inhibited by Activation of β-Adrenoceptors. Function, 3(6), zqac050.

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Long-term Administration of β-adrenergic Agonists

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For long-term administration of β-adrenergic agonists, Clenbuterol (Sigma) and BRL37344 (Sigma) were dosed at 2 mg Kg⁻¹ day⁻¹ and 2.4 mg Kg⁻¹ day⁻¹, respectively, using subcutaneously implanted Alzet osmotic pumps (model 2006; DURECT Corporation). Six weeks following implantation of the first pump, an additional pump was implanted for a total of 12 weeks of continuous drug delivery. Control animals were implanted with Alzet pumps containing saline (PBS; Gibco).

Maryanovich M., Zahalka A.H., Pierce H., Pinho S., Nakahara F., Asada N., Wei Q., Wang X., Ciero P., Xu J., Leftin A, & Frenette P.S. (2018). Adrenergic nerve degeneration in bone marrow drives aging of the hematopoietic stem cell niche. Nature medicine, 24(6), 782-791.

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Adrenergic Receptor Agonist Protocols

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SR59230A was from Santa Cruz Biotechnology, Heidelberg, Germany, and ICI-118551 from ICI-Pharma, Cheshire, UK. BRL37344 and tyramine were from Sigma Chemical Co., St. Louis, MO, USA.

, & Berg T. (2014). β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats. Frontiers in Physiology, 5, 499.

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Adipose Tissue Metabolic Regulation

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Glucose, glucose oxidase, BRL37344, DMEM, and RPMI 1640 medium were from Sigma-Aldrich (St. Louis, MO). Antibodies against Akt, phospho-Akt (Ser473), hormone-sensitive lipase (HSL), phosphor-HSL (Ser660), adipose triglyceride lipase (ATGL), peroxisome proliferator–activated receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), Ki-67, AMPK, and phosphor-AMPK (Thr172) were from Cell Signaling Technology (Danvers, MA). Antibody against mouse adiponectin was from R&D Systems (Minneapolis, MN). Anti-GAPDH, PEPCK, glucose-6-phosphatase (G6Pase), and horseradish peroxidase–linked secondary antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA). The lipoprotein lipase (LPL) activity assay kit was from Cell Biolabs (San Diego, CA). Free fatty acid (FFA) and TG assay kits ware purchased from Wako Diagnostics (Richmond, VA). NuPAGE gels, SuperScript III reverse transcriptase, and oligo(dT)_12–18 primer were from Invitrogen (Carlsbad, CA). The mouse diabetes multiplex assay kit was from Bio-Rad (Hercules, CA).

Qiao L., Wattez J.S., Lee S., Nguyen A., Schaack J., Hay WW J.r, & Shao J. (2017). Adiponectin Deficiency Impairs Maternal Metabolic Adaptation to Pregnancy in Mice. Diabetes, 66(5), 1126-1135.

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Adrenergic Receptor Stimulation in Adipose Tissue

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Tissue samples were incubated for 1 h in DMEM containing 0.5% fatty acid-free BSA (control media). To assess the response of tissue explants to adrenergic receptor stimulation the control media was supplemented with BRL, a beta₃ receptor agonist (BRL 37344; 50 ng/ml, Sigma) or BRL plus insulin (2.5 mU/ml recombinant human insulin, Sigma). Post incubation medium was collected and glycerol concentration measured. The glycerol concentration of the media was corrected for adipose tissue weight.

Thompson N., Huber K., Bedürftig M., Hansen K., Miles-Chan J, & Breier B.H. (2014). Metabolic programming of adipose tissue structure and function in male rat offspring by prenatal undernutrition. Nutrition & Metabolism, 11, 50.

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Chemical Sympathectomy and β3-Adrenergic Agonist Treatment

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Chemical sympathectomy was performed by intraperitoneal injection of 150 mg/kg 6-hydroxydopamine (6-OHDA; Sigma-Aldrich, St. Louis, MO, USA) in 0.1% ascorbic acid on three consecutive days as described before [25 (link)]. Surgical experiments were initiated on the fifth day.
Treatment with the β3-adrenergic agonist BRL37344 (Sigma, St. Louis, MO, USA) was performed by intraperitoneal injections at 2 mg/kg twice per day (every 10–12 h) as reported before [26 (link)]. The treatment was started immediately after surgery and continued until euthanasia at day 3 or 7.

Wagner J.M., Wallner C., Becerikli M., Reinkemeier F., von Glinski M., Sogorski A., Huber J., Dittfeld S., Becker K., Lehnhardt M., Dadras M, & Behr B. (2022). Role of Autonomous Neuropathy in Diabetic Bone Regeneration. Cells, 11(4), 612.

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Evaluating Bladder Function in Mice

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The experimental study was performed at the Laboratory of Experimental Surgery,
Universidade Federal do Ceará (UFC) after approval by the Ethics and Animal Research
Committee (protocol 05/14).
The sample consisted of 30 male Mus Musculus mice weighing between 40 and 50g. The
mice came from the Bioterio of UFC, and were distributed randomly in 5 groups of 6
animals. The mice were kept in polypropylene cages with galvanized zinc-plated wire
cover, coated with excelsiors. They were housed in adequate conditions of
temperature (average of 25ºC), ventilation, lighting, relative air humidity around
50% and the light and darkness alternating every 12 hours. They received water and
ad libitum feed.
Group 1 did not receive any of the medications and served as a control group. 2-5
groups received 60 mg / kg / day L-NAME (Sigma-Aldrich, St. Louis, Missouri, USA)
diluted in drinking water¹⁰. Groups 3 and 4 received 4mg / kg / day of Tadalafila (Cayman, Ann Arbor,
Michigan, USA) by oral gavage⁹. In groups 4 and 5, 5mg / kg / intraperitoneal BRL-37344 (Sigma-Aldrich, St.
Louis, Missouri, USA) was administered once every 30 minutes prior to
cystometry¹⁵. After 30 days of follow-up, all mice were referred for
cystometry.

de Carvalho M.F., Pamplona T.L., Barreira M.A., Fechine F.V., Gonzaga-Silva L.F, & de Oliveira R.R. (2019). Effect of co-administration of BRL-37344 and tadalafil on reduction of overactive bladder symptoms after induction of detrusor overactivity in mice. Acta Cirúrgica Brasileira, 34(2), e201900205.

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