Presence Of Piroxicam Research Articles

Preparation and Administration of a Controlled-Release Delivery System of Chitosan Hydrogel loaded with Methadone and Piroxicam in Experimental Defect of Tibial in Rats; Histopathological Evaluation

Purpose: In this study, a controlled-release drug delivery system loaded with piroxicam and methadone was synthesized and used subcutaneously in rats with experimental tibial defect, and healing were assessed histopathologically.
 Materials and Methods: For this purpose, 100 adult female rats were randomly divided into five equal groups; control group, chitosan group, piroxicam group, methadone group, and piroxicam-methadone group. The morphological structure of the synthesized drug systems was studied by scanning electron microscope. In addition, the structure of the hydrogels was investigated by Fourier transform infrared spectroscopy and while releasing the hydrogels' gelation time, the release of piroxicam and methadone from the hydrogels was evaluated in vitro.
 Results: Histological results of the 3rd day of the study showed the lowest extent and severity of inflammation in the chitosan, piroxicam, and piroxicam-methadone groups, while on the 7th day, tissue inflammation and the extent of bleeding were lower in the piroxicam, methadone, and piroxicam-methadone groups than in the other groups. Evaluation of new bone formation on day 21 showed that the chitosan, piroxicam, and methadone groups had better repair than the other groups.
 Conclusion: It seems that in the control group that did not receive any treatment intervention, following the experimental bone defect, the highest inflammatory response was observed in histological examination and finally the weakest bone repair. On the other hand, the presence of piroxicam, methadone, and chitosan in the piroxicam-methadone group (all of which have anti-inflammatory effects) also seems to have a negative effect on the repair.

High sensitive titanium/chitosan-coated nanoporous gold film electrode for electrochemical determination of acetaminophen in the presence of piroxicam

In this paper, the electro-catalytic activity of nano-porous gold film (NPGF) electrode modified with titanium (Ti) and chitosan (CS) is studied with regard to the determination of acetaminophen (AC) and piroxicam (PX). Underpotential deposition (UPD) is employed to cover Ti on NPGF electrode surface (TiNPGF), and then electrochemical method is used to modify the TiNPGF electrode surface using CS film (CS-TiNPGF). Scanning electron microscopy (SEM) and energy-dispersive X-ray spectroscopy (EDX) are employed for the characterization of the attained CS-TiNPGF electrode. CS-TiNPGF electrode shows great efficiency to the electrochemical oxidation of AC with a low detection limit 0.01 μM. The result acquired from differential pulse voltammetry (DPV) technique is linearly dependent on AC concentration in the ranges of 0.06–50.0 μM with a correlation coefficient of 0.9890, and in the range of 60.0–700.0 μM with a correlation coefficient of 0.9940. CS-TiNPGF electrode also shows excellent performance for determination of AC in the presence of P X . This electrode is used to find out the content of acetaminophen and piroxicam in biological and pharmaceutical samples using the standard addition method.

Corrosion Control of Mild Steel Material in HCl Electrolyte by a Non-Steroidal Anti-Inflammatory Drug: Electrochemical and Kinetic Study

The corrosion inhibition of mild steel by a drug substance, namely piroxicam, in HCl (1 M) solution was investigated. The Electrochemical Impedance Spectroscopy (EIS) and potentiodynamic polarization technique were used. EIS measurements showed larger capacitive loops in the presence of piroxicam. The inhibition efficiency was found to be dependent on the piroxicam concentration. From the polarization curves the corrosion current density ( $${{i}_{{{\text{cor}}}}}$$ ) decreased from 109.4 to 16.93 μA/cm2. The adsorption mode of the drug obeys to the Langmuir isotherm model. The free energy of adsorption (∆Gads) revealed a spontaneous process with a mixed interaction type i.e. physical and chemical. The kinetic study was conducted using the weight loss technique at the optimal piroxicam concentration (600 ppm). The density functional theory (DFT) method was used to determine the principal species, neutral or ionized drug, involved the inhibition mechanism. Scanning electron microscopy (SEM) was carried out for the surface characterization of the carbon steel after immersion in the aggressive medium in the absence and presence of the drug substance.

Application of Response Surface Methodology and Genetic Algorithm for Optimization and Determination of Iron in Food Samples by Dispersive Liquid–Liquid Microextraction Coupled UV–Visible Spectrophotometry

A simple and facile method was developed for the determination of trace amount of iron. The method is based on the complex formation between Fe (III) and picrate anion in the presence of piroxicam, as a complexing agent. Dispersive liquid–liquid microextraction (DLLME) was applied to extract the formed ion associate, Fe (III)-piroxicam. The absorbance of the extracted iron in the sedimented phase was measured by UV–Vis spectrophotometry. Two statistical methods of response surface methodology and genetic algorithm (GA) based on artificial neural network (ANN) were employed for prediction and optimization of a four-constituent DLLME. Plackett–Burman design was used for screening the influential parameters including pH, the volume of picrate anion, disperser, and extraction solvents. Central composite design (CCD) was used to obtain the optimum levels in the proposed method. The experimentally obtained data were used to train the GA model. CCD and GA models were compared for their predictive abilities. The result showed that both models have the ability to predict the proposed process, but ANN model is more reliable than CCD. The absorbance of the extracted iron obeys Beer’s law in the range of 0.03–0.96 $$\upmu \hbox {g}\,\hbox {mL}^{-1 }({R}^{2} = 0.998)$$ , and the limit of detection of 0.008 $$\upmu \hbox {g}\ \hbox {mL}^{-1}$$ and enhancement factor of 88.84 were achieved for the process. The developed procedure was successfully applied to the determination of iron in water samples and two types of common vegetation sample, i.e., tea and mint.

SYNTHETIC PRODUCT ILLEGALLY SOLD IN BRAZIL AS A MEDICINAL HERBAL PRODUCT: CHEMICAL ANALYSIS AND THE PATIENT’S MEDICATION EXPERIENCE

<pre><strong>Objective</strong>:<strong> </strong>To analyze a product illegally sold as herbal medicine acquired and used by a patient and to understand the reasons that led the patient to use this product. <strong></strong></pre><pre><strong>Methods</strong>:<strong> </strong>The chemical analysis was performed by thin layer chromatography (TLC) and mass spectrometry (MS) analysis with a direct infusion with a Bruker Daltonics UltroTOF-Q, in positive mode. A qualitative interview was conducted with the patient. The data obtained were submitted to thematic analysis. <strong></strong></pre><pre><strong>Results</strong>:<strong> </strong>Chemical analysis confirmed the presence of piroxicam and orphenadrine, and the complete absence of a natural product. The qualitative study revealed three themes: previous experience with the disease and the use of medicines, feelings about the care provided by health professionals, and the patient’s solution.<strong></strong></pre><strong>Conclusion: </strong>The commercial availability of this kind of product raises concerns about safety and demonstrates the necessity for more intensive surveillance by health authorities. In addition, the present study showed the need for a patient-centered practice and the understanding of medication experience to provide effective care to patients who use medicines to preserve them from unsafe products.

Interactions Between Sirolimus and Anti-Inflammatory Drugs: Competitive Binding for Human Serum Albumin.

The aim of the present study was investigating the effects of three anti-inflammatory drugs, on Sirolimus protein biding. The binding site of Sirolimus on human serum albumin (HSA) was also determined. Six different concentrations of Sirolimus were separately exposed to HSA at pH 7.4 and 37°C. Ultrafiltration method was used for separating free drug; then free drug concentrations were measured by HPLC. Finally, Sirolimus protein binding parameters was calculated using Scatchard plots. The same processes were conducted in the presence of NSAIDs at lower concentration of albumin and different pH conditions. To characterize the binding site of Sirolimus on albumin, the free concentration of warfarin sodium and Diazepam, site I and II specific probes, bound to albumin were measured upon the addition of increasing Sirolimus concentrations. Based on the obtained results presence of Diclofenac, Piroxicam and Naproxen, could significantly decrease the percentage of Sirolimus protein binding. The Binding reduction was the most in the presence of Piroxicam. Sirolimus-NSAIDs interactions were increased in higher pH values and also in lower albumin concentrations. Probe displacement study showed that Sirolimus may mainly bind to site I on albumin molecule. More considerations in co-administration of NSAIDs and Sirolimus is recommended.

A high sensitive biosensor based on FePt/CNTs nanocomposite/N-(4-hydroxyphenyl)-3,5-dinitrobenzamide modified carbon paste electrode for simultaneous determination of glutathione and piroxicam

This study describes the development, electrochemical characterization and utilization of novel modified N-(4-hydroxyphenyl)-3,5-dinitrobenzamide-FePt/CNTs carbon paste electrode for the electrocatalytic determination of glutathione (GSH) in the presence of piroxicam (PXM) for the first time. The synthesized nanocomposite was characterized with different methods such as TEM and XRD. The modified electrode exhibited a potent and persistent electron mediating behavior followed by well-separated oxidation peaks of GSH and PXM. The peak currents were linearly dependent on GSH and PXM concentrations in the range of 0.004–340 and 0.5–550µmolL−1, with detection limits of 1.0nmolL−1 and 0.1µmolL−1, respectively. The modified electrode was successfully used for the determination of the analytes in real samples with satisfactory results.

Role of PGE2 in the colonic motility: PGE2 generates and enhances spontaneous contractions of longitudinal smooth muscle in the rat colon

The aim of this study was to determine which PGE2 receptors (EP1-4 receptors) influence colonic motility. Mucosa-free longitudinal smooth muscle strips of the rat middle colon spontaneously induced frequent phasic contractions (giant contractions, GCs) in vitro, and the GCs were almost completely abolished by a cyclooxygenase inhibitor, piroxicam, and by an EP3 receptor antagonist, ONO-AE3-240, but enhanced by tetrodotoxin (TTX). In the presence of piroxicam, exogenous PGE2, both ONO-AE-248 (EP3 agonist), and ONO-DI-004 (EP1 agonist) induced GC-like contractions, and increased the frequency and amplitude. These effects of EP receptor agonists were insensitive to TTX and ω-conotoxins. In immunohistochemistry, the EP1 and EP3 receptors were expressed in the longitudinal smooth muscle cells. These results suggest that the endogenous PGE2 spontaneously generates and enhances the frequent phasic contractions directly activating the EP1 and EP3 receptors expressed on longitudinal smooth muscle cells in the rat middle colon.

Determination of Piroxicam in Different Pharmaceutical Products by a Simple Kinetic Procedure Based on An Induction Period Effect

In this study, a simple and sensitive induction period based kinetic spectrophotometric method is reported for determination of trace amounts of piroxicam (PX). This method is based upon the inhibition effect of PX on the catalytic oxidation of m-creosol purple (MCP) with periodate. In the presence of PX, an induction period appears in the reaction system, which is proportional to the PX concentration. The decolorization of MCP at 525 nm is used to monitor the reaction spectrophotometrically. Under the optimum conditions, PX can be determined in the range of 1–12.5 μM (0.33–4.14 μg mL-1), with a 3σ detection limit of 0.54 μM (0.18μg mL-1). The relative standard deviations for six replicate determinations of 1.25, 5.0, and 10.0 μM piroxicam are 1.03 %, 0.28 %, and 0.22 %, respectively. This method could successfully be used in the determination of PX in various pharmaceutical products.

A one-pot method to enhance dissolution rate of low solubility drug molecules using dispersion polymerization in supercritical carbon dioxide

The surfactant assisted polymerization of 1-vinyl-2-pyrrolidone in supercritical carbon dioxide in the presence of Piroxicam, selected as a model of a low aqueous solubility drug, was studied in order to prepare in a single step a polymeric composite to enhance the rate of dissolution of the pharmaceutical compound. Reactive entrapping was carried out at 65 °C in the P range 21–38 MPa. Under proper operative conditions we obtained the composite under the form of sub-micron spherical particles with relatively narrow particle size distribution. Drug loadings higher than 12% (w/w) were obtained and XRD and Raman spectroscopy suggest that the anti-inflammatory agent is dispersed in the matrix with a non-crystalline structure. The dissolution rate of the drug from the composites was significantly faster both than that of the pure compound and of its physical mixture with the polymer. Collected results suggest that the proposed one-pot process can be used to prepare polymer based composites to increase bioavailability of low solubility drugs without utilization of toxic solvents and under mild temperature conditions.

Role of prostaglandin E 2 and Ca 2+ in bradykinin induced contractions of guinea-pig gallbladder in vitro

In this study, we investigated the contribution of prostaglandin E 2 to bradykinin induced contractions of guinea-pig gallbladder in vitro and characterized the sources of activator Ca 2+ for the bradykinin mediated contractions. Contractions induced by bradykinin in guinea-pig gallbladder smooth muscle strips were significantly attenuated by the cyclooxygenase inhibitor piroxicam (10 μM). In the presence of piroxicam, a threshold concentration of prostaglandin E 2 (1 nM) significantly enhanced the contractile response to subsequent challenge with bradykinin. Contractile responses to bradykinin were abolished in a Ca 2+-free medium plus EDTA. The inhibitor of receptor mediated Ca 2+ entry, SK&F 96365 (1-[β-[3-(4-methoxyphenyl)-propoxy]-4-methoxyphenethyl]-1 H-imidazole hydrochloride, 10–50 μM) dose dependently abolished the response to bradykinin, while this response was only partially attenuated by nifedipine (10–50 μM; a voltage-operated Ca 2+ channel antagonist). Thapsigargin (an inhibitor of the sarcoplasmic reticulum calcium ATP-ase pump, 1 μM) produced sustained contractions of guinea-pig gallbladder strips that were dependent on extracellular Ca 2+. After incubation of strips in a Ca 2+-free medium with thapsigargin, replacement of Ca 2+ caused a large sustained contraction. We conclude that the contractile response of guinea-pig gallbladder to bradykinin is modulated by prostaglandin E 2. Bradykinin induced contractions of guinea-pig gallbladder are highly dependent on extracellular Ca 2+ which enters through store-operated Ca 2+ channels and partially through voltage-operated Ca 2+ channels.

Cyclic AMP and Ca2+ interactions affecting epithelial chloride secretion in human cultured colonic epithelia

1. Chloride secretion in three types of cultured epithelial monolayers derived from a single human colonic adenocarcinoma was measured in terms of short circuit current. The three cell types were designated HCA-7, Colony 3 and Colony 29. 2. Responses of HCA-7 monolayers to basolaterally applied lysylbradykinin (LBK) (10-1000 nM) or carbachol (1-100 microM) were potentiated by pre-exposure to forskolin (10 microM) for 5 min. Forskolin itself increased short circuit current (SCC), so that the total response to forskolin and LBK or carbachol were non-additive. 3. Colony 3 cells did not respond to LBK on either face but did to carbachol on the basolateral side, while Colony 29 epithelia responded to LBK on both sides and to carbachol and histamine basolaterally. Unlike HCA-7 epithelia, responses in Colony 3 and Colony 29 epithelia were not potentiated by forskolin, but were attenuated by piroxicam. 4. In the presence of piroxicam, both forskolin and prostaglandin E2 were able to potentiate the action of both LBK and carbachol in Colony 29 epithelia. 5. LBK receptor activation in Colony 29 epithelia is transduced into an increase in intracellular Ca2+ and cyclic AMP, while in HCA-7 epithelia there is only an increase in intracellular Ca2+ (Cai). These conclusions are considered to apply to both apical and basolateral kinin receptors. 6. It is shown that forskolin has no effect on the elevation of Ca2+ by LBK in either HCA-7 or Colony 29 cells. 7. It is concluded that potentiation of agonist responses occurs when cyclic AMP is raised at the time that intracellular Ca2+ increases. No potentiation of LBK or carbachol by forskolin occurs in Colony 29 monolayers as these agonists increase cyclic AMP via eicosanoid production.

A lack of pharmacokinetic interaction between ranitidine and piroxicam

The effects of piroxicam (40 mg) on the pharmacokinetics of ranitidine (150 mg) and of ranitidine (150 mg bid) on the pharmacokinetics of piroxicam (20 mg) were assessed in two 2-way crossover studies in two groups of 18 healthy male subjects. In the first study there were no statistically significant differences between the pharmacokinetic variables for ranitidine in the presence or absence of piroxicam. The mean maximum plasma concentration (Cmax) was 467 ng.ml-1 for ranitidine alone and 466 ng.ml-1 in the presence of piroxicam: mean area under the plasma concentration vs time curve (AUC) was 2460 h.ng ml-1 and 2551 h.ng ml-1 respectively; and the mean terminal half-life (t 1/2) was 3.6 h and 3.8 h respectively. In the second study there were no statistically significant differences between the pharmacokinetic variables for piroxicam in the presence or absence of ranitidine. The mean Cmax was 2.1 micrograms.ml-1 in the presence of placebo and 2.0 micrograms.ml-1 in the presence of ranitidine respectively; mean AUC was 133 h.microgram ml-1 and 137 h.microgram ml-1 respectively, and the mean t 1/2 was 53.6 h and 54.5 h respectively.

The pharmacologic regulation of interleukin-1 production: The role of prostaglandins

The role of prostaglandins in the regulation of lipopolysaccharide (LPS)-induced interleukin-1 (IL-1) production by murine C3H/HeN resident peritoneal macrophages was studied. IL-1 production was initially studied in the presence of piroxicam and indomethacin, both inhibitors of prostaglandin biosynthesis. IL-1 was assayed using the IL-1-dependent proliferative response of C3H/HeJ thymocytes. LPS stimulation resulted in 15 to 20 ng/ml of prostaglandin E 2 (PGE 2) produced in the first hour of culture. IL-1-containing supernatants from drug-treated macrophages at dilutions of up to 1:32 resulted in enhanced thymocyte proliferation compared to control, non-drug-treated cultures and contained less than 2 ng/ml of PGE 2. Similar enhancement of proliferation could be obtained by incubating non-drug-treated supernatants with monoclonal anti-PGE 2 but not anti-thromboxane B 2 (TxB 2) antibody. Further dilutions of the drug-treated supernatants gave thymocyte proliferation responses which were indistinguishable from control cultures and, correspondingly, had identical values for IL-1 production. The absence of an effect on IL-1 production was confirmed by quantitation of intracellular IL-1α using goat anti-IL-1α antibody and by quantitation of supernatant IL-1 using an IL-1 receptor competition assay. Exogenous PGE 2, in the concentration range produced in macrophage supernatants (10–20 ng/ml), directly inhibited IL-1-stimulated thymocyte proliferation. Finally, when macrophages were stimulated with LPS for 24 hr in the presence of added PGE 2, thymocyte proliferation was inhibited at the lowest supernatant dilutions, but as the IL-1-containing supernatants were diluted out, the assay curves were indistinguishable from non-PGE 2-treated control. Thus, in this system, PGE 2 has no effect on IL-1 synthesis, but rather has a direct inhibitory effect on thymocyte proliferation. Nonsteroidal anti-inflammatory drugs are not stimulating IL-1 production but are, in fact, relieving inhibition of the thymocyte IL-1 assay caused by the presence of prostaglandins.

Piroxicam in breast milk after long-term treatment.

The presence of piroxicam in breast milk was determined by HPTLC during initial and long term dosing in 4 women treated for arthritis. Piroxicam appeared in breast milk at about 1-3% of the maternal plasma concentration. No accumulation of piroxicam occurred in milk relative to that in plasma up to 52 days of treatment. Neither piroxicam nor its conjugates were detectable in the urine of one breast-fed infant. The daily dose ingested by the infant was calculated to average 3.5% (maximum 6.3%) of the weight-related maternal dose of piroxicam. It is concluded that a breast-fed infant will be exposed to a very small amount of piroxicam.

Dissociation by piroxicam of degranulation and superoxide anion generation from decrements in chlortetracycline fluorescence of activated human neutrophils

Human neutrophils (PMN), activated by appropriate stimuli, aggregate, generate O 2 • , secrete lysosomal enzymes, and exhibit a characteristic decrease in chlortetracycline (CTC) fluorescence, which has been attributed to mobilization of membrane-bound Ca, a possible requirement for stimulus-secretion coupling in PMN. Preincubation of PMN with piroxicam (50 μM) before stimulation with the chemotactic peptide f-met-leu-phe (FMLP) inhibited each of these responses. In addition, binding of 3H-FMLP was significantly reduced in the presence of piroxicam. In contrast, when either concanavalin A (Con A) or phorbol myristate acetate (PMA) were used as stimuli in the presence of piroxicam, aggregation and secretion of lysozyme proceeded normally, whereas O 2 • generation and CTC fluorescence decrements were significantly inhibited. The binding of 3H-Con A was unaffected by piroxicam. Since secretion and aggregation could be dissociated from the CTC-fluorescence response, it is unlikely that an event monitored by decrements in CTC fluorescence is necessary for stimulus-secretion coupling.