Hc 030031

Manufactured by Merck Group

Sourced in United States, Sao Tome and Principe, Germany, Italy

HC-030031 is a laboratory equipment product. It serves as a core function in scientific research and experimentation. Further details on the specific use or application of this product are not available.

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Lab products found in correlation

Capsazepine, by Merck Group (8 mentions) Capsaicin, by Merck Group (7 mentions) Ruthenium red, by Merck Group (7 mentions) A 967079, by Merck Group (5 mentions) Dimethyl sulfoxide (dmso), by Merck Group (5 mentions) Cinnamaldehyde, by Merck Group (4 mentions) Allyl isothiocyanate, by Merck Group (4 mentions) Indomethacin, by Merck Group (3 mentions) Fluo 4 am, by Thermo Fisher Scientific (3 mentions) Thapsigargin, by Merck Group (2 mentions) Pentoxifylline, by Merck Group (2 mentions) Fsllry nh2, by Merck Group (2 mentions) Sc144, by Merck Group (2 mentions) Phenylmethanesulfonyl fluoride pmsf, by Merck Group (2 mentions) Allyl isothiocyanate aitc, by Merck Group (2 mentions) Probenecid, by Merck Group (2 mentions) Nifedipine nif, by Merck Group (1 mentions) Prostaglandin e2 pge2, by Merck Group (1 mentions) Histamine his, by Merck Group (1 mentions) Verapamil, by Merck Group (1 mentions)

50 protocols using hc 030031

Intrathecal Catheter Implantation and Drug Administration in Rats

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The rats were anesthetized by sodium pentobarbital (40 mg/kg, i.p.) in order to implant intrathecal catheter for administration of drugs 3 days prior to each experiment. Briefly, one end of polyethylene-10 tubing was inserted intrathecally through an incision in the cisternal membrane and advanced 7-9 cm caudal until the tip of the catheter was positioned at the lumbar spinal level (L5 to L6). The other end of the intrathecal tubing was sutured to the musculature and skin at the incision site and externalized to the back of the rat. In each experiment, a Hamilton microsyringe (250 µl) was connected to the intrathecal tubing and used to deliver 100 μl of dimethyl sulfoxide (DMSO) as control, FSLLRY-NH2 (PAR2 antagonist, 10 μg), SB366791 (TRPV1 antagonist, 100 μM) and HC030031 (TRPA1 antagonist, 10 μg) (Kanai et al. 2006 ) (obtained from Sigma-Aldrich).
In a subset of studies, in order to examine the effects of PAR2 on expression of TRPV1 and TRPA1 and engagement of substance P and CGRP FSLLRY-NH2 (10 μg), SB366791 (100 μM) and HC030031 (10 μg) were intrathecally given using an infusion pump in control rats and rats 4 weeks following SCI, respectively. The pump was set to constantly deliver vehicle or the drugs over a period of 3 h. At the end of infusion, the superficial dorsal horn tissues were obtained under an anatomical microscope for Western Blot and ELISA experiments.

Wei H., Wei Y., Tian F., Niu T, & Yi G. (2016). Blocking proteinase-activated receptor 2 alleviated neuropathic pain evoked by spinal cord injury. Physiological research, 65(1).

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Investigating Ion Channel Modulators

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The following reagents were used: allyl-isothiocyanate, (AITC, Sigma), 4-(3-chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide (BCTC, Sigma), bradykinin (BK), capsaicin (Caps, Alomone Labs), ω-conotoxin GIVA (Ascent scientific), forskolin (Fors, Abcam), HC-030031 (Sigma), Histamine (His, Sigma), nifedipine (Nif, Sigma), oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC, Hycultech), PGPC (Avanti Polar Lipids), prostaglandin E2 (PGE₂, Sigma), tetrodotoxin (TTX, Ascent scientific). Dimethyl sulfoxide, chloroform or aqueous physiological solutions served as solvents.

Martin C., Stoffer C., Mohammadi M., Hugo J., Leipold E., Oehler B., Rittner H.L, & Blum R. (2018). NaV1.9 Potentiates Oxidized Phospholipid-Induced TRP Responses Only under Inflammatory Conditions. Frontiers in Molecular Neuroscience, 11, 7.

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Krebs-Henseleit Physiological Salt Solution Protocol

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The physiologic salt solution used was Krebs-Henseleit, which had the following
composition: 118.0 mmol/L NaCl, 4.7 mmol/L KCl, 2.5 mmol/L CaCl₂, 1.2
mmol/L MgSO₄, 25.0 mmol/L NaHCO₃, 1.2 mmol/L
KH₂PO₄, 10.0 mmol/L glucose). Solutions with high KCl
content involved addition of appropriate amounts of a 3-M KCl solution (in distilled
water) directly to the organ bath to achieve the desired concentration. For some
experiments, barium ions (Ba²⁺) substituted for Ca²⁺ in the
physiologic salt solution.
(±)-β-Citronellol (95% purity; Code C83201), ACh (PubChem ID 24891113), atropine (ID
24890401), 5-hydroxytryptamine (ID 24278124), L-N^G-nitroarginine methyl
ester (L-NAME; ID 24278011), tetraethylammonium (TEA; ID 24277874), sodium
orthovanadate (ID 24899708), capsazepine (ID 24277967), indomethacin (INDO; ID
24278173), A-967079 (CAS Number 1170613-55-4), HC-030031 (CAS Number 349085-38-7),
thapsigargin (ID 24278762) and verapamil (ID 24277881) were purchased from
Sigma-Aldrich (USA).
In general, stock solutions were prepared in distilled water and stored at -20°C.
β-Citronellol was dissolved directly in physiologic solution containing 2% Tween 80
and sonicated immediately before addition in the bath chamber. The maximum
concentration of the vehicle in the organ bath was 0.01% (v/v).
Salts (all of analytical grade) were purchased from Sigma-Aldrich or Merck
(Germany).

Vasconcelos T.B., Ribeiro-Filho H.V., Lucetti L.T, & Magalhães P.J. (2015). β-Citronellol, an alcoholic monoterpene with inhibitory properties on the contractility of rat trachea. Brazilian Journal of Medical and Biological Research, 49(2), e4800.

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Neuropathic Pain Management in Rats

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All animal protocols were in accordance with the guidelines of the International Association for the Study of Pain and approved by the Research Committee of our institution. In order to minimize experimental bias due to the sex difference, both genders of Wistar rats (200-250 g; 50% male vs. 50% female) were housed in individual cages with free access to food and water. The animals were kept in a temperaturecontrolled room (25°C) on a 12/12 h light/dark cycle.
A model of neuropathic pain and administration of drugs BTZ (0.4 mg/kg body weight; Haoran BioTech Co., Shanghai, China; Cat#B1408) was administrated intraperitoneally (i. p.) once daily for 5 consecutive days on the basis of previous reports [16, 19] . Control animals received an equivalent volume of saline. After BTZ intervention, TRPA1 antagonist HC030031 (1, 3, 10 mg/kg body weight; Sigma, St. Louis, MO, US; Product#H4415/CAS#349085-38-7) was administrated i.p. each day for the following 3 consecutive days. In the same fashion, a TNF-α synthesis inhibitor, pentoxifylline (PTX, 10, 20 and 40 mg/kg body weight; Sigma, St. Louis, MO, US; Product# P1784/CAS#6493-05-06) was given i.p. each day for 3 consecutive days.

Li C., Deng T., Shang Z., Wang D, & Xiao Y. (2018). Blocking TRPA1 and TNF-α Signal Improves Bortezomib-Induced Neuropathic Pain. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 51(5).

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Pharmacological Tools for Pain Research

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Capsaicin, formalin, prostaglandin E2, thapsigargin, picrotoxin, lidocaine, γ‐aminobutyric acid (GABA), muscimol (3‐hydroxy‐5‐aminomethyl‐isoxazole), HC‐030031 (1,2,3,6‐tetrahydro‐1,3‐dimethyl‐N‐ [4‐ (1‐methylethyl) phenyl] ‐ 2,6‐dioxo‐7H‐purine‐7‐acetamide), bumetanide (3‐(aminosulfonyl)‐5‐(butylamino)‐4‐phenoxy benzoic acid), AH23848 ((4Z)‐7‐[(rel‐1S,2S,5R)‐5‐((1,1′‐biphenyl‐4‐yl)methoxy)‐2‐(4‐morpholinyl)‐3‐oxocyclopentyl]‐4‐heptenoic acid hemicalcium salt), AH6809 (6‐isopropoxy‐9‐oxoxanthene‐2‐carboxylic acid) and A887826 (5‐(4‐butoxy‐3‐chlorophenyl)‐N‐[[2‐(4‐morpholinyl)‐3‐pyridinyl]methyl]‐3‐pyridinecarboxamide) were purchased from Sigma. For in vivo experiments, formalin and muscimol were dissolved in 0.9% saline with sonication. For in vivo experiments, AH6809, A887826, bumetanide, and capsaicin were dissolved in 100% DMSO as stocks at 10 mmol/L and AH23848 was dissolved in saline +2% DMSO; all drugs were further diluted in bath solution immediately before experiments.

Jang I.J., Davies A.J., Akimoto N., Back S.K., Lee P.R., Na H.S., Furue H., Jung S.J., Kim Y.H, & Oh S.B. (2017). Acute inflammation reveals GABAA receptor‐mediated nociception in mouse dorsal root ganglion neurons via PGE 2 receptor 4 signaling. Physiological Reports, 5(8), e13178.

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Evaluating Combinatorial Inhibitory Treatments for Cancer

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Two weeks after inoculation of cancer cells, a TNF-α synthesis inhibitor,
pentoxifylline (PTX, 10, 20, and 40 mg/kg body weight; Sigma), and SC144, an
inhibitor to complexed IL-6R-gp130 (5, 10, and 20 mg/kg body weight; Sigma),
were given i.p., individually, each day for three consecutive days. In the same
manner, TRPA1 antagonist HC030031 (1, 3, 10, mg/kg body weight; Sigma) was
administrated i.p. each day for the following three consecutive days.

Zhao D., Han D.F., Wang S.S., Lv B., Wang X, & Ma C. (2019). Roles of tumor necrosis factor-α and interleukin-6 in regulating bone cancer pain via TRPA1 signal pathway and beneficial effects of inhibition of neuro-inflammation and TRPA1. Molecular Pain, 15, 1744806919857981.

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Masseter Muscle Pharmacological Modulation

Cited 2 times

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For behavioral experiments, NMDA (10 μmol/40 μl), a specific agonist for the NMDAR, and alpha,beta-methylene adenosine triphosphate (αβmeATP) (750 μg/20 μl, pH adjusted to 7.0 using NaOH), a specific agonist for P2X₃, were dissolved in phosphate buffered saline (PBS). AP18 (10 nmol to 2 μmol), a TRPA1 antagonist, was dissolved in 1% DMSO, 10% Tween-80, and 89% PBS. HC-030031 (50 nmol), another TRPA1 antagonist, was dissolved in 10% DMSO. NMDA, αβmeATP and HC-030031 were purchased from Sigma-Aldrich (St. 6 Louis, MO). AP18 was purchased from Enzo Life Sciences (Farmingdale, NY). Doses of NMDA, αβmeATP, and AP18 were adapted from our previous studies (Ro et al., 2009 (link), Lee et al., 2012b (link), Saloman et al., 2013 (link)). All drugs were administered directly into the masseter muscle.

Asgar J., Zhang Y., Saloman J.L., Wang S., Chung M.K, & Ro J.Y. (2015). The role of TRPA1 in muscle pain and mechanical hypersensitivity under inflammatory conditions in rats. Neuroscience, 310, 206-215.

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Evaluation of TRPA1 and TRPV1 Agonists

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Both agonist candidates (cinnamaldehyde, natural, ≥95%, Food grade; capsaicin, ≥95%) and their blockers (HC-030031, ≥98%, HPLC-grade; capsazepine, ≥98%, HPLC-grade) were obtained from Sigma-Aldrich, Castle Hill, New South Wales, Australia. Dimethyl sulfoxide (DMSO) and phenylmethanesulfonylfluoride (PMSF) were purchased from Sigma-Aldrich (Castle Hill, New South Wales, Australia). Chemicals to make Krebs-Ringer buffer (KRB) (D-glucose (1.8 g L⁻¹), magnesium chloride (0.0468 g L⁻¹), potassium chloride (0.34 g L⁻¹), sodium chloride (7.0 g L⁻¹), sodium phosphate dibasic (0.1 g L⁻¹), sodium phosphate monobasic (0.18 g L⁻¹), HEPES (5.957 g L⁻¹)) were purchased from Sigma-Aldrich (Castle Hill, New South Wales, Australia). The pH of the KRB buffer was adjusted to pH 7.4 before use.

Van Liefferinge E., Müller M., Van Noten N., Degroote J., Niknafs S., Roura E, & Michiels J. (2021). Cinnamaldehyde Induces Release of Cholecystokinin and Glucagon-Like Peptide 1 by Interacting with Transient Receptor Potential Ankyrin 1 in a Porcine Ex-Vivo Intestinal Segment Model. Animals : an Open Access Journal from MDPI, 11(8), 2262.

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Evaluating TRPA1 Antagonist Efficacy in Swallowing Reflex

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HC-030031 (Wako Pure Chemical Industries Ltd., Osaka, Japan) was used as a TRPA1 antagonist. HC-030031 is a well-known TRPA1 antagonist. The efficacy of HC-030031 in blocking TRPA1s was previously valiadted^{68 (link)–70}. HC-030031 was dissolved in a small amount of DMSO (1%; Sigma-Aldrich, St. Louis, MO) and Tween 80 (1%; Sigma-Aldrich) and was diluted with saline. The corresponding DMSO/Tween 80/saline solution was used as the vehicle. Pilot experiments were performed to determine the lowest effective concentrations of HC-030031 that attenuated the number of swallowing reflexes to ≤ 50% of that triggered by the 2.5 mM AITC. The lowest effective concentrations of HC-030031 that attenuated the number of AITC-induced swallowing reflexes to ≤ 50% was 2 mM. Therefore, we used 2 mM HC-030031 in the remaining experiments where the effect of TRPA1 antagonist on the AITC-induced swallowing reflexes was tested. We used 2 mM and 5 mM HC-030031 in the experiments where the effect of TRPA1 antagonist on the mechanical stimuli-induced swallowing reflexes was tested. The number of AITC-induced/mechanical stimuli-induced swallowing reflexes was counted 10 min following application of the TRPA1 antagonist or vehicle.

Hossain M.Z., Ando H., Unno S, & Kitagawa J. (2022). TRPA1s act as chemosensors but not as cold sensors or mechanosensors to trigger the swallowing reflex in rats. Scientific Reports, 12, 3431.

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TRPA1 Silencing and TGF-β1 Activation in Myofibroblasts

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Licorice extract powder was dissolved in ethanol by sonication and purified by filtering. AITC and HC-030031 were obtained from Sigma-Aldrich (St. Louis, MO). Recombinant human TGF-β1 (Wako, Osaka, Japan) was added to cultured cells according to the manufacturer’s instructions. Human Stealth small interfering RNAs (siRNAs) for TRPA1 (TRPA1HSS113276 (5′-GGAGCAAUUGCUGUUUACUUCUAUU-3′ and 5′-AAUAGAAGUAAACAGCAAUUGCUCC-3′) were obtained from Invitrogen (Carlsbad, CA) and used for gene silencing according to the manufacturer’s instructions. Other TRPA1-siRNAs, TRPA1HSS113277 and TRPA1HSS189723, also were evaluated, but the silencing efficacy was inferior to that by TRPA1HSS113276 for InMyoFibs. Antibodies against TRPA1 (mouse, Sigma-Aldrich; rabbit, Novus, CO), HSP47 (rabbit; Abcam, Cambridge, UK), α-SMA (Abcam), β-actin (Abcam), collagen I (Abcam), Smad-2/3, and phospho-Smad-2 (Cell Signaling Technology, Danvers, MA) were used for immunoblotting and immunostaining experiments. The human TRPA1 plasmid used for single-channel recording was kindly provided by Professor Yasuo Mori (Kyoto University, Japan).

Kurahara L.H., Hiraishi K., Hu Y., Koga K., Onitsuka M., Doi M., Aoyagi K., Takedatsu H., Kojima D., Fujihara Y., Jian Y, & Inoue R. (2017). Activation of Myofibroblast TRPA1 by Steroids and Pirfenidone Ameliorates Fibrosis in Experimental Crohn's Disease. Cellular and Molecular Gastroenterology and Hepatology, 5(3), 299-318.

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