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Aicar

Manufactured by Abcam
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AICAR is a chemical compound that functions as an AMP-activated protein kinase (AMPK) activator. AMPK is an important cellular energy sensor and regulator. AICAR can alter cellular metabolism and signaling pathways.

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Lab products found in correlation

Compound c, by Merck Group (3 mentions) Ex 527, by Merck Group (2 mentions) Hydrogen peroxide, by Merck Group (2 mentions) Simvastatin, by Merck Group (2 mentions) N acetylcysteine, by Merck Group (2 mentions) Etomoxir, by Merck Group (2 mentions) Mk 2206, by Cayman Chemical (2 mentions) Allopurinol, by Merck Group (2 mentions) Oleic acid, by Cayman Chemical (2 mentions) Diphenyleneiodonium chloride dpi, by Merck Group (2 mentions) D4902, by Merck Group (2 mentions) Cerulenin, by Merck Group (2 mentions) L ng nitroarginine methyl ester l name, by Cayman Chemical (2 mentions) Sirt1 activator 2, by Merck Group (2 mentions) Af 214 14, by Thermo Fisher Scientific (2 mentions) 25 hydroxycholesterol, by Cayman Chemical (2 mentions) Hmgcoa, by Merck Group (2 mentions) Cholesterol methyl β cyclodextrin, by Merck Group (2 mentions) Ly294002, by Thermo Fisher Scientific (1 mentions) Tgf β1, by Thermo Fisher Scientific (1 mentions)

7 protocols using aicar

1

Polarization of Bone Marrow-Derived Macrophages

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BMMФ were stimulated either with IL-4 (10 ng/ml, AF-214-14, Peprotech), lipopolysaccharide (100 ng/ml, Sigma) or dexamethasone (100nM, D4902, Sigma) to respectively achieve M(IL-4), M(LPS) or M(GC) polarization state. In some experiments, BMMФ were treated with C75 (Sigma), Cerulenin (Sigma), Etomoxir (Sigma), pan-AKT inhibitor MK-2206 (1 mM, Cayman Chemical), 25-hydroxycholesterol (10 μM, Cayman chemical), N-acetyl cysteine (10mM, Sigma), Diphenyleneiodonium chloride (DPI, 5 μM, Sigma), L-NG-Nitroarginine methyl ester (L-NAME, 1mM, Cayman Chemical), Allopurinol (100 μM, Sigma), hydrogen peroxide (Sigma), SIRT1 activator II (Sigma), EX-527 (Sigma), Compound C (Sigma), AICAR (Abcam), HMGCoA (Sigma), water-soluble cholesterol (Cholesterol–methyl-β-cyclodextrin, Sigma) or Simvastatin (Sigma).
For fatty acid treatment, palmitic or oleic acid (Cayman) were solubilized at 100mM in absolute ethanol at 60°C. Fatty acid were conjugated at the desired concentration using a sonicator water bath into the macrophage culture medium to avoid endotoxin contamination from BSA54 (link).
Bidault G., Virtue S., Petkevicius K., Jolin H.E., Dugourd A., Guénantin A.C., Leggat J., Mahler-Araujo B., Lam B.Y., Ma M.K., Dale M., Carobbio S., Kaser A., Fallon P.G., Saez-Rodriguez J., McKenzie A.N, & Vidal-Puig A. (2021). SREBP1-induced fatty acid synthesis depletes macrophages antioxidant defences to promote their alternative activation. Nature metabolism, 3(9), 1150-1162.
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2

Neuromuscular Coculture and IGF-1 Effects

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The SKM cell cultures and sensory innervation cultures were treated as follows: (1) SKM group: The SKM cells were cultured for 2 days with SKM medium, and the culture continued for another 4 days with coculture medium; (2) SKM + DRG group: SKM cells were cultured for 2 days and were then cocultured for another 4 days with DRG explants; (3) SKM + IGF-1 group: The SKM cells were cultured for 2 days with SKM medium, 2 days with coculture medium, and another 2 days with coculture medium containing IGF-1 (20 nmol/L); and (4) Coculture + IGF-1 group: The SKM cells were cultured for 2 days in SKM medium and another 4 days with coculture medium with DRG explants; IGF-1 (20 nmol/L) was applied in the last 2 days. After processing for the live monitoring of mitochondrial morphology, real-time PCR and Western blot assays of the SKM cells, the SKM + DRG + IGF-1 group was treated with either the PI3K inhibitor LY294002 (10 μmol/L, Invitrogen), Mul1 overexpression lentivirus, or the AMPKα activator AICAR (1 mmol/L, Abcam) for further exploration of the mechanisms underlying the effects of IGF-1 on SKM cells in neuromuscular cocultures.
Ding Y., Li J., Liu Z., Liu H., Li H, & Li Z. (2017). IGF-1 potentiates sensory innervation signalling by modulating the mitochondrial fission/fusion balance. Scientific Reports, 7, 43949.
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3

AICAR Modulates TGF-β1-Induced Corneal Fibrosis

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In vitro analyses were performed by directly stimulating primary corneal fibroblasts with TGF-β1 to induce fibrosis. The fibroblasts were seeded into culture plates and allowed to attach. The cells were pretreated with 0.5-mM and 1-mM AICAR (Abcam, Cambridge, UK) dissolved in dimethyl sulfoxide for 2 to 3 hours followed by 5 ng/mL TGF-β1 (PeproTech, Seoul, Korea) and then incubated. To determine if the observed effects were AMP-activated protein kinase (AMPK) dependent, the cells were pretreated for 2 hours with 2.5-µM and 5-µM Compound C (Merck, Darmstadt, Germany), an AMPK antagonist, followed by 1-mM AICAR for 2 hours and then 5-ng/mL TGF-β1, and then incubated. The incubation periods were 8 hours for the detection of signaling proteins and 48 hours for the detection of ECM proteins.
Nuwormegbe S.A, & Kim S.W. (2020). AMPK Activation by 5-Amino-4-Imidazole Carboxamide Riboside-1-β-D-Ribofuranoside Attenuates Alkali Injury-Induced Corneal Fibrosis. Investigative Ophthalmology & Visual Science, 61(6), 43.
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4

Polarization of Bone Marrow-Derived Macrophages

Cited 1 time
Check if the same lab product or an alternative is used in the 5 most similar protocols
BMMФ were stimulated either with IL-4 (10 ng/ml, AF-214-14, Peprotech), lipopolysaccharide (100 ng/ml, Sigma) or dexamethasone (100nM, D4902, Sigma) to respectively achieve M(IL-4), M(LPS) or M(GC) polarization state. In some experiments, BMMФ were treated with C75 (Sigma), Cerulenin (Sigma), Etomoxir (Sigma), pan-AKT inhibitor MK-2206 (1 mM, Cayman Chemical), 25-hydroxycholesterol (10 μM, Cayman chemical), N-acetyl cysteine (10mM, Sigma), Diphenyleneiodonium chloride (DPI, 5 μM, Sigma), L-NG-Nitroarginine methyl ester (L-NAME, 1mM, Cayman Chemical), Allopurinol (100 μM, Sigma), hydrogen peroxide (Sigma), SIRT1 activator II (Sigma), EX-527 (Sigma), Compound C (Sigma), AICAR (Abcam), HMGCoA (Sigma), water-soluble cholesterol (Cholesterol–methyl-β-cyclodextrin, Sigma) or Simvastatin (Sigma).
For fatty acid treatment, palmitic or oleic acid (Cayman) were solubilized at 100mM in absolute ethanol at 60°C. Fatty acid were conjugated at the desired concentration using a sonicator water bath into the macrophage culture medium to avoid endotoxin contamination from BSA54 (link).
Bidault G., Virtue S., Petkevicius K., Jolin H.E., Dugourd A., Guénantin A.C., Leggat J., Mahler-Araujo B., Lam B.Y., Ma M.K., Dale M., Carobbio S., Kaser A., Fallon P.G., Saez-Rodriguez J., McKenzie A.N, & Vidal-Puig A. (2021). SREBP1-induced fatty acid synthesis depletes macrophages antioxidant defences to promote their alternative activation. Nature metabolism, 3(9), 1150-1162.
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5

Pharmacological Modulators of Neuronal Signaling

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Cells were treated before collection or imaging with AICAR (1 mM, 2 h, Abcam), CC (20 µM, 2 h, Abcam), AKT inhibitor VIII (10 µM, 2 h, TCI), GSK1904529A (1 µM, 2 h, Abcam), Wortmannin (1 µM, 2 h, EMD Millipore), CCCP (20 µM, 2 h, Sigma-Aldrich, insulin (500 nM, 1 h, Sigma-Aldrich), Torin-2 (10 nM, 30 min, Sigma-Alrich), AA (5 nM or 20 µM, 45 min, Alfa Aesar), ApoE3 or E4 (50 nM, overnight, PeproTech). The compounds were either dissolved in water (AICAR, CC, insulin, ApoE3 and E4), in dimethylsulfoxide (DMSO; AKT inhibitor VIII, GSK1904529A; Wortmannin, CCCP and Torin-2) or ethanol (AA). For compounds dissolved in DMSO or ethanol, control samples were treated with the same amount of the respective solvent. For insulin starvation, neurons were cultured for 2 h or overnight in NB + B27 + PSG lacking insulin.
Hees J.T., Wanderoy S., Lindner J., Helms M., Murali Mahadevan H, & Harbauer A.B. (2024). Insulin signalling regulates Pink1 mRNA localization via modulation of AMPK activity to support PINK1 function in neurons. Nature Metabolism, 6(3), 514-530.
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6

AICAR Preparation and Administration

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AICAR was obtained from Abcam (Cambridge, UK) (ab120358, Lot: APN12423-1-1;) for cell experiments, and LC Laboratories (Woburn, MA, USA) (A-1098, Lot: ACR-101) for animal experiments. AICAR was dissolved in distilled water and immediately stored at −20°C. This stock solution was diluted in culture medium for in vitro or saline for in vivo experiments, immediately before use.
Morishita M., Kawamoto T., Hara H., Onishi Y., Ueha T., Minoda M., Katayama E., Takemori T., Fukase N., Kurosaka M., Kuroda R, & Akisue T. (2016). AICAR induces mitochondrial apoptosis in human osteosarcoma cells through an AMPK-dependent pathway. International Journal of Oncology, 50(1), 23-30.
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7

AICAR Mimics Exercise in HLMVEC

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HLMVEC were treated with 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR; Abcam) to mimic the effect of exercise. AICAR is a cell-permeable activator of AMP-activated protein kinase (AMPK). Before stretching, HLMVEC were treated with AICAR (10 mM) for 24 h to simulate exercise.
YAN J., GU C., LIU G., ZHANG Y., YANG L., ZHAO T., CAO C., ZHAO L., WU G, & WANG Y. (2023). Aerobic Exercise in Male Mice Prevents Ventilator-Induced Lung Injury by Inhibiting Mitochondrial Damage from sirt1 Dysregulation. Medicine and Science in Sports and Exercise, 55(10), 1770-1780.
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