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Glibenclamide

Manufactured by Merck Group
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Glibenclamide is a medication used as a lab equipment product. It is a sulfonylurea drug that helps regulate blood sugar levels. The core function of Glibenclamide is to stimulate the release of insulin from the pancreas, which can be useful in research and laboratory settings.

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Lab products found in correlation

Indomethacin, by Merck Group (26 mentions) Streptozotocin (stz), by Merck Group (21 mentions) L name, by Merck Group (17 mentions) Dimethyl sulfoxide (dmso), by Merck Group (16 mentions) Acetylcholine, by Merck Group (16 mentions) Apamin, by Merck Group (14 mentions) Diazoxide, by Merck Group (13 mentions) Potassium chloride (kcl), by Merck Group (13 mentions) Nifedipine, by Merck Group (12 mentions) Phenylephrine, by Merck Group (11 mentions) 4 aminopyridine 4 ap, by Merck Group (11 mentions) Barium chloride, by Merck Group (10 mentions) Pinacidil, by Merck Group (9 mentions) 4 aminopyridine, by Merck Group (9 mentions) D glucose, by Merck Group (9 mentions) Adenosine triphosphate (atp), by Merck Group (9 mentions) Glimepiride, by Merck Group (9 mentions) Charybdotoxin, by Merck Group (9 mentions) Tolbutamide, by Merck Group (8 mentions) Sucrose, by Merck Group (8 mentions)

Spelling variants of this product

Glibenclamide (GLB) (5 citations) Glibenclamide (GB) (3 citations) Glibenclamide (Gli) (2 citations) Glibenclamide (Glib) (2 citations)

240 protocols using glibenclamide

1

Preparation and Use of Chemical Reagents

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Nifedipine, glibenclamide, acetylcholine, sodium pentobarbital, bovine serum albumin (BSA), HEPES, DL-Dithiothreitol (DTT), and 6-propyl-2-thiouracil (PTU) were purchased from Sigma (St. Louis, MO, USA); collagenase P, NADP disodium salt, ATP disodium salt, glucose-6-phosphate dehydrogenase from Roche (Roche Diagnostic, Mannheim, Germany), and all other reagent-grade chemicals from Merck (Darmstadt, Germany).
Stock solutions of Nifedipine and glibenclamide, were prepared in ethanol and dimethyl sulphoxide (DMSO) and the other substances were dissolved in H2O or directly added into the incubation media.
Godini A., Ghasemi A, & Zahediasl S. (2015). The Possible Mechanisms of the Impaired Insulin Secretion in Hypothyroid Rats. PLoS ONE, 10(7), e0131198.
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2

Investigating Vasoactive Substances in Tissue

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Quercetin (2‐(3,4‐Dihydroxyphenyl)‐3,5,7‐trihydroxy‐4H‐1‐benzopyran‐4‐one) was purchased from abcr GmbH (Karlsruhe, Germany), while Carbamylcholine chloride ((2‐Hydroxyethyl)trimethylammonium chloride carbamate; carbachol), N5‐(Nitroamidino)‐L‐2,5‐diaminopentanoic acid, NG‐NO2‐L‐Arg (Nω‐Nitro‐L‐arginine, L‐NNA), NG‐Methyl‐L‐Arg (Nω‐Nitro‐L‐arginine methyl ester hydrochloride, L‐NAME), cystamine, pinacidil, 1H‐[1,2,4]Oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ), apamin, charybdotoxin (CTX), glibenclamide, and tamoxifen were purchased from the Sigma Chemical Company, were purchased from Sigma (St. Louis, MO).
Quercetin, ODQ, and glibenclamide were dissolved in in dimethyl sulfoxide (DMSO) so that the final concentration of DMSO was never >0.1%, which had no effect on basal contraction. Dilution series of Quercetin were prepared on the day of experiment and were sustained at room temperature during the period of the experiment.
Stock solutions of carbachol, L‐NNA, L‐NAME, cystamine, pinacidil, apamin, CTX, and tamoxifen were prepared using bidistilled water. All substances were added directly to the organ bath containing a Tyrode's solution composed of (mmol/L): NaCl 139.6; KCl 2.68; MgCl2 1.05; NaH2PO4 1.33; CaCl2 1.80; NaHCO3 25.0; and glucose 5.55.
Modzelewska B., Drygalski K., Kleszczewski T., Chomentowski A., Koryciński K., Kiełczewska A., Pawłuszewicz P, & Razak Hady H. (2021). Quercetin relaxes human gastric smooth muscles directly through ATP‐sensitive potassium channels and not depending on the nitric oxide pathway. Neurogastroenterology and Motility, 33(7), e14093.
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3

Pharmacological Modulation of Myocardial Ischemia

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Pinacidil (Sigma-Aldrich CO) was dissolved in ethyl alcohol (96%) and then mixed with isotonic solution and it was given in 0.1 mg/0.2 ml / kg doses intravenously from a coccygeal tail vein 10 min before coronary ligation. Glibenclamide (Sigma-Aldrich CO) was dissolved in dimethylsulfoxide and then mixed with ethanol in the same ratio (1/1).
Glibenclamide was given in 5 mg/0.2 ml/kg doses intraperitoneally 20 min before coronary ligation. In the control group, instead of the Pinacidil and Glibenclamide, the same value of solvent 0.2 ml/kg was applied in both regions. The doses of both drugs used in this study were chosen according to the studies performed previously (21 ). Since Pinacidil was also a hypotensive agent, larger doses usually lead to the dead of animals due to bradycardia and cardiac arrest. Otherwise glybenclamide is more effective in 5 mg/kg dose in intraperitoneal injection. Lower doses of Glibenclamide which were tested in previous study were found to be ineffective on ischemia induced arrhythmia (10 ).
Yaşar S., Bozdoğan Ö., Kaya S.T, & Orallar H.S. (2015). The effects of ATP-dependent potassium channel opener; pinacidil, and blocker; glibenclamide, on the ischemia induced arrhythmia in partial and complete ligation of coronary artery in rats. Iranian Journal of Basic Medical Sciences, 18(2), 188-193.
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4

Apoptosis Measurement of Virus-Transduced Cells

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Cellular apoptosis was measured by a RealTime-Glo Annexin V Apoptosis and Necrosis assay kit (Promega) according to the manufacturer’s instructions. Briefly, 1 × 104 cells/well were seeded into a 96-well plate and cultured at 37°C/5% CO2 overnight. After viral transduction with the Adv control or Adv-Vpr, the detection reagent (which included Annexin V NanoBiT substrate, CaCl2, Necrosis Detection Reagent, Annexin V-SmBiT, and Annexin V-LgBiT) was added into each well of a 96-well plate. Following incubation at 37°C/5% CO2, at the indicated time frame the luminescence (relative light units [RLU]) and fluorescence (RFU, 485nmEx/520–30nmEm) were measured for apoptosis at different time points with a SYNERGY-H1 microplate reader. A stock solution of glibenclamide was prepared by placing 25 mg glibenclamide (number G2539; meets USP testing; Sigma-Aldrich) into 10 ml dimethyl sulfoxide (DMSO).
Li G., Makar T., Gerzanich V., Kalakonda S., Ivanova S., Pereira E.F., Andharvarapu S., Zhang J., Simard J.M, & Zhao R.Y. (2020). HIV-1 Vpr-Induced Proinflammatory Response and Apoptosis Are Mediated through the Sur1-Trpm4 Channel in Astrocytes. mBio, 11(6), e02939-20.
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5

Glibenclamide Toxicology Protocol

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Glibenclamide (Sigma-Aldrich, CAS N° 10238–21–8) was used as the test substance for in vitro and in vivo tests. Glibenclamide was dissolved in 1% dimethyl sulfoxide (DMSO CAS n° 67–68–5) supplied by Sigma-Aldrich (St.Louis, Mo, USA), which was also tested as solvent control. Mitomycin-C (CAS n° 50–07–7, St. Louis, MO), used as the positive control for the MNvit test, cytosine arabinoside (CAS n° 205–705–9, St. Louis, MO), used in the in vivo homozygotization assay, and cytochalasin B (CAS n° 14930–96–2, St. Louis, MO) were also purchased from Sigma. RPMI 1640 cell culture media supplemented with L-glutamine (11875–093), fetal bovine serum (12657–029) and phytohemagglutinin (10576–015) were purchased from Gibco Life Technologies. Giemsa and all other chemicals were purchased from Merck (Darmstadt, Germany). All test solutions were freshly prepared before each experiment. All chemicals, solvents and culture media used in this study were of the highest purity.
de Sant’Anna J.R., Franco C.C., Mathias P.C, & de Castro-Prado M.A. (2015). Assessment of In Vivo and In Vitro Genotoxicity of Glibenclamide in Eukaryotic Cells. PLoS ONE, 10(3), e0120675.
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6

Caspase Inhibitors and Mitochondrial Modulators

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Soluble recombinant human TRAIL was obtained from Enzo Life Sciences (San Diego, CA, USA). The general caspase inhibitor, z-VAD-FMK, and caspase-3/7-specific inhibitor, z-DEVD-FMK, were purchased from Merck Japan (Tokyo, Japan). Glibenclamide, FCCP, antimycin A and U37883A were from Sigma-Aldrich (St. Louis, MO, USA). Potassium chloride (KCl) was obtained from Wako Pure Chemicals (Osaka, Japan). Insoluble reagents (z-VAD-FMK, z-DEVD-FMK, Glibenclamide, FCCP, antimycin A and U37883A) were dissolved in dimethyl sulfoxide (DMSO) and diluted with high glucose-containing Dulbecco’s modified Eagle’s medium (DMEM; Sigma-Aldrich) supplemented with 10% fetal bovine serum (FBS; Sigma-Aldrich) or Hank’s balanced salt solution (HBSS) (pH 7.4) to a final concentration of <0.1% prior to use. The manganese-porphyrin superoxide dismutase mimetic MnTBaP (Enzo Life Sciences) were dissolved in 1 mM NaOH (pH 8.0) and added HBSS to lower pH 7.4.
Tokunaga T., Ando T., Suzuki-Karasaki M., Ito T., Onoe-Takahashi A., Ochiai T., Soma M, & Suzuki-Karasaki Y. (2018). Plasma-stimulated medium kills TRAIL-resistant human malignant cells by promoting caspase-independent cell death via membrane potential and calcium dynamics modulation. International Journal of Oncology, 52(3), 697-708.
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7

Glibenclamide Treatment for EAE Mice

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After the onset of clinical symptoms (>20 % of WT/EAE mice with clinical scores of 1 or greater; pid-10), 10 μg glibenclamide was administered daily by IP injection to WT/EAE mice in the treatment group until the end of the experiment (pid-30). A stock solution of glibenclamide was prepared by placing 25 mg of glibenclamide (#G2539; meets USP testing; Sigma, St. Louis, MO) into 10 mL dimethyl sulfoxide (DMSO). We diluted 200 μL of this solution in 9.8 mL PBS; mice received 100 μL of this solution.
Makar T.K., Gerzanich V., Nimmagadda V.K., Jain R., Lam K., Mubariz F., Trisler D., Ivanova S., Woo S.K., Kwon M.S., Bryan J., Bever C.T, & Simard J.M. (2015). Silencing of Abcc8 or inhibition of newly upregulated Sur1-Trpm4 reduce inflammation and disease progression in experimental autoimmune encephalomyelitis. Journal of Neuroinflammation, 12, 210.
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8

Pharmacological Modulation of Cellular Pathways

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Citral, metformin (a hypoglycemic drug), naltrexone and naloxone (both opioid receptors blockers), NG-L-nitro-arginine methyl ester (L-NAME)(a NO synthase inhibitor), 1 H-(1,2,4)-oxadiazolo (4,2-a) quinoxalin-1-one (ODQ)(a NO-sensitive soluble guanylyl cyclase inhibitor), glipizide and glibenclamide (both ATP-sensitive K + channel blockers; K ir 6.1-2), 4-aminopyridine (4-AP) and tetraethylammonium chloride (TEA) (both voltage-gated K + channel blockers; K V ), charybdotoxin (a big conductance Ca 2+ -activated K + channel blocker; K Ca 1.1), and apamin (a small conductance Ca 2+ -activated K + channel blocker; K Ca 2.1-3) were acquired from Sigma-Aldrich (Toluca, Mexico).
glibenclamide, glipizide and ODQ were dissolved in a 20% DMSO solution. L-NAME, TEA, 4-AP, apamin, charybdotoxin, naloxone, naltrexone and metformin were dissolved in saline solution.
Ortiz M.I., Cariño-Cortés R., Muñoz-Pérez V.M., Medina-Solís C.E, & Castañeda-Hernández G. (2022). Citral inhibits the nociception in the rat formalin test: effect of metformin and blockers of opioid receptor and the NO-cGMP-K+ channel pathway. Canadian journal of physiology and pharmacology, 100(4).
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9

Cardioprotective Effects of Remote Conditioning

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I. Rats in control group were subjected to 30-min ischemia (occlusion of LAD coronary artery) followed by 3-h reperfusion (re-opening the LAD coronary artery). II. Rats in pre-conditioning group were subjected to remote pre-conditioning procedure: 5-min femoral artery occlusion followed by 1-min re-opening of the artery, which was repeated for three times before LAD coronary artery occlusion. III. Rats in per-conditioninggroup were subjected to remote per-conditioning procedure: 5-min femoral artery occlusion followed by 1-min re-opening of the artery, which was repeated for three times during LAD coronary artery occlusion.
IV. Rats in naloxone group were received the same treatment as per-conditioning procedure and an injection of naloxone (1.0 mg. kg -1 , Sigma), an antagonist of opioid receptors, 5 min before per-conditioning procedure.
V. Rats in glibenclamide group were received the same treatment as per-conditioning procedure and an injection of glibenclamide (1.0 mg.kg -1 , Sigma), an antagonist of K ATP channels, 5 min before per-conditioning procedure.
Zhang L., Guo H., Yuan F., Hong Z.C., Tian Y.M., Zhang X.J, & Zhang Y. (2018). Limb remote ischemia per-conditioning protects the heart against ischemia-reperfusion injury through the opioid system in rats. Canadian journal of physiology and pharmacology, 96(1).
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10

Hippocampal Glibenclamide Effect on APP/PS1 Mice

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Guide cannula implantation and in vivo microdialysis were performed as described above. Glibenclamide (100 μM; MilliporeSigma) was infused directly into the hippocampus of Kir6.2+/+ APP/PS1 mice, Kir6.2–/– APP/PS1 mice, and Kir6.1–/– APP/PS1 mice (n = 4–7) via reverse microdialysis for 3 hours. Changes in ISF glucose, lactate, and Aβ were quantified as described below. Statistical significance was determined using a 1-way ANOVA and Dunnett’s multiple-comparison post hoc test. Data are represented by means ± SEM.
Grizzanti J., Moritz W.R., Pait M.C., Stanley M., Kaye S.D., Carroll C.M., Constantino N.J., Deitelzweig L.J., Snipes J.A., Kellar D., Caesar E.E., Pettit-Mee R.J., Day S.M., Sens J.P., Nicol N.I., Dhillon J., Remedi M.S., Kiraly D.D., Karch C.M., Nichols C.G., Holtzman D.M, & Macauley S.L. (2023). KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer’s disease–related pathology. JCI Insight, 8(10), e162454.
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