Male and female IL‐10–/– mice were randomly divided into four groups: the control group, piroxicam group, 5‐ASA group (100 mg kg−1 d−1) and POL group (400 mg kg−1 d−1). The piroxicam group, 5‐ASA group, and POL group were administered 200 ppm piroxicam (P0847, Sigma‐Aldrich) in feed for 14 d to induce colitis, while the control group was given normal mouse chow.[21 ] Simultaneously, the 5‐ASA and POL groups were given 5‐ASA and POL, respectively, by gavage starting on the first day. The control and piroxicam groups were administered equal doses of normal saline. Another six wild‐type C57BL/6 mice served as the wild‐type group. According to the Meeh‐Rubner formula, the conversion coefficient between human and mouse doses is 1:8,[22 ] the mice dose of 5‐ASA and POL equates to human dose of 12.5 and 50 mg kg−1 d−1. For an individual with a body mass of 60 kg, to achieve this dose they would need to consume 0.75 g of 5‐ASA or 3 g POL per day.
Piroxicam
Manufactured by Merck Group
Sourced in United States, United Kingdom, Germany, Denmark, Brazil, Italy
Piroxicam is a laboratory analytical instrument used for the detection and quantification of piroxicam, a non-steroidal anti-inflammatory drug (NSAID). It is designed to provide accurate and reliable measurements of piroxicam concentrations in various samples, such as biological fluids or pharmaceutical formulations.
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62 protocols using piroxicam
1
Colitis Induction and Treatment Protocol
2
Piroxicam in IL-10 deficient mice
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3
Piroxicam's Neuroprotective Effects in MCAO Rats
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Ninety-six male Charles Foster rats, aged 6 weeks, weighing 270 ± 10 g, were used for the experiments. Rats were kept under standard laboratory conditions. These rats were fasted overnight and maintained at a 12-hour light/dark cycle. Then they were divided into blank control (n = 6), middle cerebral artery occlusion (MCAO; n = 6) and MCAO + Piroxicam (n = 84) groups. MCAO was performed according to a previously described method (Bhattacharya et al., 2014). Rats in the MCAO + Piroxicam group were administered Piroxicam (Sigma-Aldrich, St. Louis, MO, USA; 10 mg/kg body weight, i.p.), which was pre-dissolved in normal saline, 30 minutes prior to MCAO (Bhattacharya et al., 2013). Fourteen time points were selected to optimize the baseline in vehicle and drug-treated vehicle (in triplicate). The rats that either did not show significant reduction in cerebral blood flow by 70 % or died during surgery or after surgery before completing the experimental time frame were excluded from the study. The approved standard procedures and the institutional animal ethical committee guidelines of Banaras Hindu University, India were followed throughout the experiments (Approval No. 542/AB/CPCSEA).
4
Inflammatory Pain Induction and Pharmacological Modulation
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To induce cutaneous inflammation CFA (Sigma–Aldrich, Germany), was injected into the plantar surface of one hind paw (20 μl/paw). Carrageenan (Sigma–Aldrich, Germany) (100 μl/paw) was administered in separate cohorts of mice as an additional model of cutaneous tissue injury and inflammation, griess reagent, gabapentin (5 mg/kg), tramadol (50 mg/kg), piroxicam (5 mg/kg) (Merck, Darmstadt, Germany), dexamethasone (5 mg/kg), chloroform, distilled water, 2% DMSO were of research grade. Honokiol was isolated as previously described (Park et al., 2009 (link)) (10 mg/kg i.p.) dissolve in 2% DMSO and normal saline was administered before CFA or Carrageenan induced inflammation. Elisa kits of TNF-α and IL-1β (Thermo Fisher Scientific, United States), NF-κB (p65) (Cayman Chemical, Ann Arbor, MI, United States).
5
Evaluating Solubility of Diverse Pharmaceutical Compounds
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Sodium taurocholate, cholesterol, sodium chloride (NaCl), sodium oleate, ammonium formate, potassium hydroxide (KOH), hydrochloric acid (HCl), naproxen, phenytoin, piroxicam, fenofibrate, probucol, griseofulvin, carvedilol, tadalafil, and indomethacin were purchased from Merck Chemicals Ltd. Aprepitant and felodipine were provided through OrBiTo by Dr. R. Holm, Head of Preformulation, Lundbeck, Denmark. Zafirlukast was purchased from Stratech Scientific Ltd. Phosphatidylcholine from soybean (lecithin) was purchased from Lipoid company. Chloroform from Rathburn Chemical Company. FaSSIF-v1 media was purchased from Biorelevant.com Ltd. Sodium phosphate monobasic monohydrate (NaH2PO4·H2O) and formic acid from Fisher Scientific. All acetonitrile (ACN) and methanol (MeOH) solvents were HPLC gradient (VWR). All water was ultrapure Milli-Q.
6
Piroxicam-Loaded Alginate-Pectin Hydrogels
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Piroxicam, alginate sodium (Alg-Na), pectin, acetone, isopropyl alcohol, chloride calcium, potassium dihydrogenphosphat, sodium hydroxide, potassium chloride and formalin were obtained from Merck (Darmstadt, Germany). All solvents and reagents were of analytical grade.
7
Pharmaceutical Compound Characterization Protocol
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Active pharmaceutical ingredients of studied medicines, i.e., atenolol (Daroupakhsh, Iran), benzoic acid (Merck, Iran), carbamazepine (Arastoo, Iran), carvedilol (Salehan Shimi, Iran), Ibuprofen (Daana, Iran), ketoconazole (Arastoo, Iran), lamotrigine (Arastoo, Iran), phenothiazine (Merck, Germany), phenytoin (Alhavi, Iran), piroxicam (Zahravi, Iran) salicylic acid (Merck, Germany), sulfamethoxazole (Merck, Germany), and tadalafil (Osveh, Iran), were provided from pharmaceutical and chemical companies (Purity: > 99%). Ethanol (96% w/w) was purchased from Jahan Alcohol (Iran), and choline chloride (> 99%), glycerol (> 99%), and urea (> 99%) from Merck (Germany). Lab-made double distilled water was used for the preparation of solutions.
8
In Vitro Solubility Screening Compounds
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Antipyrine, cimetidine, clotrimazole, N-desmethyl-tamoxifen hydrochloride, furosemide, hydrochlorothiazide, ketoprofen, maleic acid, (+/−)-metoprolol-(+)-tartrate, (+/−)-norverapamil hydrochloride, piroxicam, tamoxifen, terbutaline hemisulfate and (+/−)-verapamil hydrochloride 99% were purchased from Sigma-Aldrich (St. Louis, MO, USA); (+/−)-propranolol hydrochloride and ranitidine hydrochloride were obtained from Alfa Aesar GmbH & Co KG (Karlsruhe, Germany), and carbamazepine was purchased from Acros Organics (New Jersey, USA). Midazolam and α-hydroxyMidazolam were purchased from Lipomed AG (Arlesheim, Switzerland), and agar, calcium chloride dihydrate, glucose hydrate, magnesium chloride hexahydrate, potassium chloride, sodium chloride, sodium hydroxide, sodium phosphate monobasic and sodium hydrogencarbonate were obtained from Hänseler AG (Herisau, Switzerland). Sodium taurocholate was purchased from Prodotti Chimici e Alimentari S.p.A., (Basaluzzo, Italy) and lecithin (grade EPCS > 98% phospholipids) was obtained from Lipoid GmbH (Ludwigshafen, Germany).
9
Piroxicam-Induced Colitis in IL-10 Knockout Mice
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Eight- to twelve-week-old IL-10 gene-deficient male (IL-10-/-) mice on C57BL/6 genetic background were bred in the animal care facility at Toulouse (INSERM US 006 ANEXPLO/CREFRE, Toulouse, France). Colitis was accelerated/synchronized by adding 150 mg kg−1 piroxicam, a non-steroidal anti-inflammatory drug, into standard chow diet for 10 days (SAFE, Scientific Animal Food & Engineering, Rosenberg, Germany) [13 (link)]. Mice were intraperitoneally injected with 200 µL of either PBS or 10 mg mL−1 naloxone-methiodide (Sigma Chemical Co., St. Louis, MO, USA) (2 mg/mouse) two days apart for the ten days of piroxicam treatment [63 (link),66 (link)].
10
Induction and Treatment of PAC IL-10 KO Model
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For induction of the PAC IL-10 k.o. model, IL-10 k.o. mice had unrestricted access to piroxicam (Sigma Aldrich, Broendby, Denmark) containing 200 ppm homogenized in 1324 Altromin diet (Altromin, Lage, Germany) from day 0 of study initiation until day 10 (first and second experiment, see Figure 6 ), and from day 0 until they reached 7.5% weight loss (third experiment). Subsequently, mice were switched to normal Altromin 1324 chow as previously described [36 (link),37 (link)].
In the second experiment, PAC mice were treated with mouse growth hormone (mGH) (30 mg/kg) or vehicle twice daily. The control treatment groups received Anti-IL-12p40 (25 mg/kg) or rat IgG2a (25 mg/kg) three times a week after termination of piroxicam treatment.
In the third experiment, PAC mice were treated with long-acting PEG-hGH (30 mg/kg), vehicle, Anti-IL-12p40 (25 mg/kg) or rat IgG2a (25 mg/kg) day 1, 3, 6 and 9 after termination of piroxicam treatment. Anti-IL-12p40 and rat IgG2a were purchased from BioXcell (West Lebanon, NH, USA) and mGH and PEG-hGH were produced in-house by Novo Nordisk (Bagsværd, Denmark).
In the second experiment, PAC mice were treated with mouse growth hormone (mGH) (30 mg/kg) or vehicle twice daily. The control treatment groups received Anti-IL-12p40 (25 mg/kg) or rat IgG2a (25 mg/kg) three times a week after termination of piroxicam treatment.
In the third experiment, PAC mice were treated with long-acting PEG-hGH (30 mg/kg), vehicle, Anti-IL-12p40 (25 mg/kg) or rat IgG2a (25 mg/kg) day 1, 3, 6 and 9 after termination of piroxicam treatment. Anti-IL-12p40 and rat IgG2a were purchased from BioXcell (West Lebanon, NH, USA) and mGH and PEG-hGH were produced in-house by Novo Nordisk (Bagsværd, Denmark).
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