Chelerythrine

Manufactured by Bio-Techne

Sourced in United Kingdom

Chelerythrine is a chemical compound derived from the plant Chelidonium majus. It is a potent and selective inhibitor of protein kinase C (PKC), which plays a critical role in various cellular processes. Chelerythrine has been widely used as a research tool to investigate the functions of PKC in biological systems.

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Lab products found in correlation

8 protocols using chelerythrine

Pharmacological Modulators of Neuronal Signaling

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The following drugs were used in the present study: the NK₁R agonist GR73632 (Sakurada et al., 1999 (link)), PI3K-Akt pathway inhibitor LY294002 (Xiao et al., 2018 (link)), PKC inhibitors chelerythrine and GF109203X (Cho et al., 2001 (link)) (the latter more selectively targets PKCα/β (Asehnoune et al., 2005 (link))), and store-operated Ca²⁺ entry (SOCE) inhibitors YM-58483 and MRS-1845 were purchased from Tocris, Minneapolis, MN. CaMKII inhibitor KN93, ERK1/2 pathway inhibitor U0126 were obtained from Calbiochem, San Diego, CA. The L-type Ca²⁺ channel blocker nifedipine was from Sigma/RBI (St. Louis, MO). The ryanodine receptor antagonist dantrolene, the inositol-1, 4, 5-triphosphate receptor (IP₃R) antagonist 2-APB were purchased from Santa Cruz (Dallas,Texas). The 5-HT₃ receptor antagonist palonosetron and NK₁ receptor antagonist netupitant were kindly provided by Helsinn Health Care (Lugano, Switzerland). GR73632 and palonosetron were dissolved in water. Nifedipine, dantrolene, 2-APB, YM-58483, MRS-1845, U0126, LY294002, chelerythrine and GF109203X were dissolved in 25% DMSO in water. Netupitant was dissolved in a 1:1:18 solution of emulphor™, ethanol and saline. All drugs were administered at a volume of 0.1 ml/10 g of body weight.

Zhong W., Chebolu S, & Darmani N. (2018). Intracellular emetic signaling cascades by which the selective neurokinin type 1 receptor (NK1R) agonist GR73632 evokes vomiting in the least shrew (Cryptotis parva). Neurochemistry international, 122, 106-119.

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Pharmacological Modulation of Insular LTD

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The drugs used in this study include: DHPG, Chelerythrine, KT5720 and KN62. Among them, Chelerythrine and DHPG were dissolved in distilled water, while KT5720 and KN62 were prepared in dimethyl sulfoxide (DMSO) as stock solutions for frozen aliquots at -20°C. All these drugs were diluted from the stock solutions to the final desired concentration in the artificial cerebrospinal fluid (ACSF) before immediate use. The diluted DMSO in ACSF had no effect on baseline synaptic transmission and plasticity. Chelerythrine, KT5720 and KN62 were purchased from Tocris Cookson (Bristol, UK) and DHPG was obtained from Abcam Biochemicals (Cambridge, UK). The doses for each compound were chosen based on our preliminary experiments and on relevant information from previous papers [38 (link),44 (link),77 (link)]. For the pharmacological rescue of insular LTD, DHPG (20 μM) with or without the drugs was bath applied for 20 min and then washed out for 30 min prior to LTD induction.

Liu M.G, & Zhuo M. (2014). Loss of long-term depression in the insular cortex after tail amputation in adult mice. Molecular Pain, 10, 1.

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Hippocampal Neuron Cholesterol Modulation

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The following compounds were added to cell medium of hippocampal neurons: Cholesterol oxidase (Choox; Calbiochem ref.: 228250; 10 IU/ml); K252a (Tocris ref.: 1683; 1 μM); SB203580 (Shelleckchem ref.: S1076; 20 μM); PH797804 (Axon Medchem ref.: 1837; 2 μM); H89 (Tocris ref.: 2910; 50 μM); Chelerythrine (Tocris ref.: 1330; 10 μM); XL-184 (Tocris ref.: 5422; 1 μM); BAPTA-AM (Invitrogen ref.: B-6769, 10 μM). Experiments with the antioxidants cocktail in cultured hippocampal neurons used: N-Acetyl-L-Cysteine (NAC, Sigma-Aldrich ref.: A7250, 5 mM) and L-Glutathione reduced (GSH, Sigma-Aldrich ref.: G4251, 5 mM). Hippocampal slices were treated with Cholesterol oxidase (Choox; Calbiochem ref.: 228250; 10 IU/ml) for Cholesterol removal. Experiments for Cholesterol addition conducted in hippocampal slices were performed at 25°C. Methyl-β-cyclodextrin-Cholesterol (MβCD-Ch) solution was prepared freshly at use concentration in ACSF, containing 30 μM Cholesterol Water-soluble (Sigma-Aldrich ref.: C4951) and 5 μM Cholesterol (Sigma-Aldrich ref.: C3045).

Martín-Segura A., Casadomé-Perales Á., Fazzari P., Mas J.M., Artigas L., Valls R., Nebreda A.R, & Dotti C.G. (2019). Aging Increases Hippocampal DUSP2 by a Membrane Cholesterol Loss-Mediated RTK/p38MAPK Activation Mechanism. Frontiers in Neurology, 10, 675.

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Pharmacological Inhibitors for Neurological Research

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The PKA inhibitor 6~22 amide (PKI) was purchased from Calbiochem (La Jolla, CA). D-AP5, DNQX, bicuculline, CGP 52432, myristoylated form of PKI, and the PKC inhibitor chelerythrine were purchased from Tocris (Bristol, UK). Other chemicals were purchased from Sigma (St. Louis, MO, USA).

Joo K., Yoon S.H., Rhie D.J, & Jang H.J. (2014). Phasic and Tonic Inhibition are Maintained Respectively by CaMKII and PKA in the Rat Visual Cortex. The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology, 18(6), 517-524.

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Neurochemical Receptor Assay Protocols

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Ethanol was purchased from Pharmco-AAPER (Brookfield, CT). Dopamine hydrochloride, sulpiride, SCH23390, nomifensine, N-[3-([1,1-Biphenyl]-4-yloxy)-3-(4-fluorophenyl)propyl]-N-methylglycine (NFPS), nisoxetine hydrochloride bicuculline, chelerythrine and Gö6976 were purchased from Tocris Biosciences (Minneapolis, MN). The cDNA plasmid pZac2.1-GfaABC1D-hPMCA2w/b-mCherry was purchased from Addgene (plasmid #111568) and used to generate an AAV2/5 virus (Univ. of South Carolina Viral Core, Columbia, SC). The AAV5-GfaABC1D-tdTomato virus was purchased from Addgene. U73122 was purchased from Abcam (Cambridge, MA). Strychnine, VU0134992 hydrochloride, sulforhodamine 101 and all reagents used to prepare aCSF, sucrose-containing and internal pipette solution were purchased from Sigma (St. Louis, MO).

Nimitvilai-Roberts S., Gioia D., Zamudio P.A, & Woodward J.J. (2021). Ethanol inhibition of lateral orbitofrontal cortex neuron excitability is mediated via dopamine D1/D5 receptor-induced release of astrocytic glycine. Neuropharmacology, 192, 108600.

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Pharmacological Interventions in Pain Research

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3,5-Diamino-N-(aminoiminomethyl)-6-chloropyrazinecarboxamide hydrochloride (Amiloride), (2E)-N-(2,3-Dihydro-1,4-benzodioxin-6-yl)-3-[4-(1,1-dimethylethyl)phenyl]-2-propenamide (AMG9810), Chelerythrine, 2′,3′–O–(2,4,6-Trinitrophenyl)adenosine-5′-triphosphate triethylammonium salt (TNP-ATP), 2′-Deoxy-N6-methyladenosine 3′,5′-bisphosphate tetrasodium salt (MRS2179) and [[(1R,2R,3S,4R,5S)-4-[6-Amino-2-(methylthio)-9H-purin-9-yl]-2,3-dihydroxybicyclo[3.1.0]hex-1-yl]methyl] diphosphoric acid mono ester trisodium salt (MRS2365) were purchased from Tocris (Ellisville, MO, USA). Amiloride, TNP-ATP, MRS2179 were dissolved in saline, respectively. AMG9810 was dissolved in 10% ethyl alcohol. Chelerythrine was dissolved in 5% DMSO. A 30 μl volume of one of the above drugs was injected intraplantarly for individual experiments.

Kwon S.G., Roh D.H., Yoon S.Y., Moon J.Y., Choi S.R., Choi H.S., Kang S.Y., Han H.J., Beitz A.J., Oh S.B, & Lee J.H. (2014). Acid evoked thermal hyperalgesia involves peripheral P2Y1 receptor mediated TRPV1 phosphorylation in a rodent model of thrombus induced ischemic pain. Molecular Pain, 10, 2.

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Cellular Signaling Pathway Assay

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N-Methyl-D-Aspartic Acid, 2′-7′-Dichlorofluoroscein, 2′-7′-Dichlorofluoroscein diacetate and Apocynin were purchased from Sigma Aldrich (St. Louis, MO). Wortmannin and Chelerythrine were purchased from Tocris Biosciences (Ellisville, MO). Sterile Saline was purchased from B. Braun Medical (Irvine, CA). Dihydroethidium (DHE) was purchased from Life Sciences (Grand Island, NY).

McGee M.A, & Abdel-Rahman A.A. (2014). Enhanced Vascular PI3K/Akt-NOX Signaling Underlies the Peripheral NMDAR-Mediated Pressor Response in Conscious Rats. Journal of cardiovascular pharmacology, 63(5), 395-405.

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Muscle Conductance Measurements

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As previously detailed (De Luca et al., 2005 and Pierno et al., 2007) , the EDL and Sol muscles were placed in a 25 mL muscle bath, maintained at 30°C and perfused with normal or chloride-free physiological solution (gassed with 95% O 2 and 5% CO 2 ; pH= 7.2-7.3). By means of standard two- injected by the current electrode. So, we experimentally determined R m and its reciprocal in physiological solution as the total conductance (g m ) and in chloride-free solution to measure the potassium conductance (gK) (Pierno et al., 2006) . The mean gCl was estimated as the mean gm minus the mean gK. Chelerythrine (Tocris Bioscience) was applied in vitro on EDL muscles dissected from control and treated rats and gCl was measured 30 min after drug addition. Briefly, the mechanical threshold (MT) for contraction was measured using a two microelectrode "point" voltage clamp method (Pierno et al., 2006) . Details are given in the Supplementary Methods.

Camerino G.M., De Bellis M., Conte E., Liantonio A., Musaraj K., Cannone M., Fonzino A., Giustino A., De Luca A., Romano R., Camerino C., Laghezza A., Loiodice F., Desaphy J.F., Conte Camerino D, & Pierno S. (2016). Statin-induced myotoxicity is exacerbated by aging: A biophysical and molecular biology study in rats treated with atorvastatin. Toxicology and applied pharmacology, 306.

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