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PubMedDate not supplied

Responses of neutrophils and lymphocytes in the cold stress: effects of nonsteroid anti-inflammatory drugs.

The cold stress induced in rabbits by lowering their body temperature by 3 degrees C resulted in neutrophilia and a decrease in number of phagocytes and phagocytized bacteria. The stress did not affect the number of lymphocytes and the ability of forming E rosettes by T lymphocytes, but depressed the formation of EAC rosettes by B lymphocytes. This inhibition of neutrophil activity was antagonized completely by acetylsalicylic acid, and substantially by mefenamic acid and indomethacin administered, in doses inhibiting pyrogen-induced fever, either 2.5 h before or 1.5 h after the hypothermia. The drugs did not antagonize the depression of the ability of formation of EAC rosettes.

Animals↗
PubMed2000

Simultaneous analysis of anthranilic acid derivatives in pharmaceuticals and human urine by high-performance liquid chromatography with isocratic elution.

A high-performance liquid chromatographic (HPLC) method for simultaneous determination of mefenamic acid (MFA), flufenamic acid (FFA) and tolfenamic acid (TFA) is presented for application to pharmaceuticals and human urine. Isocratic reversed-phase HPLC was employed for quantitative analysis using tetra-pentylammonium bromide (TPAB) as an ion-pair reagent. Urine samples were purified by solid-phase extraction using a silica-based strong anion-exchanger, Bond-Elut SAX cartridge. The HPLC assay was carried out using a Wakosil ODS 5C18 column (5 microm, 150x4.6 mm I.D.). The mobile phase consisted of 1.9 g of TPAB dissolved in 1:1 of a mixture of acetic acid-sodium acetate buffer solution, pH 5.0, and acetonitrile (11:9, v/v). The calibration curves of MFA, FFA and TFA showed good linearity in the concentration range of 33-167 microg/ml with a wavelength of 280 nm for pharmaceuticals, and in the low concentration range (1.7-30.1 microg/ml) with a wavelength of 230 nm for biological fluids. The correlation coefficients were better than 0.9999 in all cases. The lower limits of detection (defined as a signal-to-noise ratio of about 3) were approximately 2 ng for MFA, 3.5 ng for FFA and 2.5 ng for TFA. The procedure described here is rapid, simple, selective and is suitable for routine analysis of pharmaceuticals and pharmacokinetic studies in human urine samples.

Calibration↗
PubMed1979

Anti-inflammatory drugs in experimental atherosclerosis. Part 4. Inhibition of atherosclerosis in vivo and thromboxane synthesis and platelet aggregation in vitro.

Groups of New Zealand white male rabbits were fed atherogenic diets containing 1% cholesterol. The diets of experimental groups were supplemented additionally with either aspirin, phenylbutazone, mefenamic acid, flufenamic acid, oxyphenylbutazone or aminopyrine. Blood cholesterol and phospholipids were measured at 3--4 week intervals. After 12 weeks the animals were sacrificed and the severity of atherosclerosis in the thoracic aorta was measured. In separate experiments, rabbit platelets were incubated with each of the drugs individually and conversion of [14C]arachidonic acid to thromboxanes and related compounds was assayed. Inhibition of collagen and arachidonic acid-induced platelet aggregation by each drug was also measured. All drugs inhibited thromboxane synthesis and platelet aggregation in varying degrees with flufenamate and aspirin being most and aminopyrine least effective. The pattern of metabolite formation from [14C]arachidonate was consistent with a block in the cyclooxygenase reaction. Phenylbutazone, flufenamic acid and oxyphenylbutazone produced significant reductions in atherosclerotic plaque formation without major changes in blood cholesterol levels or blood cholesterol--phospholipid ratios. Aspirin and aminopyrine were ineffective. The results indicate that the effectiveness of anti-inflammatory drugs as inhibitors of thromboxane synthesis and platelet aggregation in vitro does not afford a sufficient predictive index of their anti-atherogenicity in vivo. The significance of these findings is discussed in terms of the possible involvement of cyclooxygenase derivatives in atherogenesis.

Aminopyrine↗
PubMed1998

Effect of interleukin 1 beta-induced fever on hepatic drug metabolism in rat.

1. A fever-induced model in rat was created by repeated injection of interleukin 1 beta (IL-1 beta) in the cerebroventricle and the influence of fever on hepatic drug metabolism was investigated. Fever apparently decreased the content of cytochrome P450 (CYP) and the activities of NADPH-ferrihaemoprotein reductase (fp2), aminopyrine N-demethylase, aniline hydroxylase, FAD-monooxygenase, p-nitrophenol UDP-glucuronosyl-transferase and glutathione S-transferase. Immunoblot analysis of the CYP isozymes indicated that CYP2C11 and CYP3A were extensively decreased in the IL-1 beta-induced fevered rat. 2. Repeated administration (5 days) of mefenamic acid in the fevered rat could not restore the activities of fp2, aminopyrine N-demethylase and aniline hydroxylase to control levels, although their hyperthermic state had been improved. The CYP content in the mefenamic acid-treated fevered rat was also lower than that in the control. 3. These findings suggest that fever impairs the hepatic drug-metabolizing capacity (both oxidation and some conjugations) and that the fever-induced impairments are partially retained, even if the hyperthermia has been offset by the administration of antipyretics.

Aminopyrine N-Demethylase↗
PubMed2003

Epigallocatechin-3-gallate increases intracellular [Ca2+] in U87 cells mainly by influx of extracellular Ca2+ and partly by release of intracellular stores.

Green tea has been receiving considerable attention as a possible preventive agent against cancer and cardiovascular disease. Epigallocatechin-3-gallate (EGCG) is a major polyphenol component of green tea. Using digital calcium imaging and an assay for [3H]-inositol phosphates, we determined whether EGCG increases intracellular [Ca2+] ([Ca2+]i) in non-excitable human astrocytoma U87 cells. EGCG induced concentration-dependent increases in [Ca2+]i. The EGCG-induced [Ca2+]i increases were reduced to 20.9% of control by removal of extracellular Ca2+. The increases were also inhibited markedly by treatment with the non-specific Ca2+ channel inhibitors cobalt (3 mM) for 3 min and lanthanum (1 mM) for 5 min. The increases were not significantly inhibited by treatment for 10 min with the L-type Ca2+ channel blocker nifedipine (100 nM). Treatment with the inhibitor of endoplasmic reticulum Ca2+-ATPase thapsigargin (1 micro M) also significantly inhibited the EGCG-induced [Ca2+]i increases. Treatment for 15 min with the phospholipase C (PLC) inhibitor neomycin (300 micro M) attenuated the increases significantly, while the tyrosine kinase inhibitor genistein (30 micro M) had no effect. EGCG increased [3H]-inositol phosphates formation via PLC activation. Treatment for 10 min with mefenamic acid (100 micro M) and flufenamic acid (100 micro M), derivatives of diphenylamine-2-carboxylate, blocked the EGCG-induced [Ca2+]i increase in non-treated and thapsigargin-treated cells but indomethacin (100 micro M) did not affect the increases. Collectively, these data suggest that EGCG increases [Ca2+]i in non-excitable U87 cells mainly by eliciting influx of extracellular Ca2+ and partly by mobilizing intracellular Ca2+ stores by PLC activation. The EGCG-induced [Ca2+]i influx is mediated mainly through channels sensitive to diphenylamine-2-carboxylate derivatives.

Calcium↗
PubMed1975

A sensitive method for the comparative bioassay of nonsteroidal anti-inflammatory compounds in adjuvant-induced primary inflammation in the rat.

A method for the comparative bioassay of nonsteroidal anti-inflammatory agents is presented which exploits the early inflammation induced by injection of adjuvant into the plantar surface of a hind paw of the rat. The inflammation reaches a peak on the 4th postinjection day. Daily treatment with nonsteroidal anti-inflammatory agents reduces paw volumes and the associated impairment of body growth with optimal improvement on the 4th postinjection day. In this model, phenylbutazone has shown significant activity at doses as low at 1.33 mg/kg/day. Statistically valid comparative assays conducted at dose levels equivalent to or below those used in human therapy yield potency ratios with relatively narrow confidence limits. Potencies relative to phenylbutazone for inhibiting primary adjuvant-induced inflammation are: aminopyrine, 0.066 (0.36-0.11)95%; aspirin, 0.087 (0.039-0.19)95%; mefenamic acid, 0.98 (0.64-1.6)95%; flufenamic acid, 13 (7.4-26)95%; meclofenamic acid, 23(16-33)95%; and indomethacin, 53 (35-82) 95%. Ancillary and sometimes quantitative information is also provided by the improvement in well being of the animals as reflected in body weight changes with treatment.

Aminopyrine↗
PubMed1976

Effect of anti-inflammatory drugs on lipase in vitro.

Mefenamic acid, and to a lesser extent, flufenamic acid have a significant inhibitory effect on lipolysis as determined by the action of mouse pancreas lipase on the dilauric (didodecanoic) acid ester of fluorescein. Ibuprofen, fenoprofen calcium, phenylbutazone, oxyphenbutazone and alclofenac had comparatively little effect.

Animals↗
PubMed1976

Mefanamic acid blood and urine levels in the horse determined by derivative gas-liquid chromatography-electron capture.

Mefenamic acid is extracted from biological fluids and is acylated with pentafluoropropionic anhydride to form a derivative possessing high electron affinity. The derivative is analyzed by gas-liquid chromatography with an electron capture detector. The method is particularly valuable for determining drug levels in blood where small sample and/or drug concentrations are available.

Animals↗
PubMed1992

Characterization of cytoplasmic T3 binding sites by adsorption to hydroxyapatite: effects of drug inhibitors of T3 and relationship to glutathione-S-transferases.

To facilitate studies of thyroid hormone (T3) binding to cytoplasmic proteins, we prepared monkey (M. fascicularis) liver cytosol (100,000g supernatant) and examined T3 binding using hydroxyapatite (HAP) separation. HAP adsorbs cytoplasmic and nuclear binding sites but not serum T4 binding proteins. Cytosol was incubated with [125I]T3 for 30 min at 4 degrees C and separated by adding an equal volume of HAP (15 g/100 mL). After a further incubation of 10 min, the HAP pellet was washed three times in buffer containing Triton X-100, 0.5%. With this method, a single class of T3 binding site was observed with Kd 15.8 +/- 1.2 nM, concentration 0.62 +/- 0.17 pmol/mg protein (n = 3, mean +/- SD). We used this assay to assess potential drug inhibitors of cytoplasmic binding and to evaluate the proposal that glutathione-S-transferases (GST) and cytoplasmic T3 binding proteins are identical. Displacement of [125I]T3 by unlabeled iodothyronines relative to T3 (100) was T4 58, Triac 7, rT3 7, Tetrac less than or equal to 1. This hierarchy indicates that this binding site is distinct from nuclear or serum binding sites. T3 binding was displaceable by nonsteroidal anti-inflammatory drugs (NSAID) and nonbile acid cholephils (NBAC). Half-inhibitory concentrations (microM, mean +/- SD, n greater than or equal to 3) were diclofenac 4.9 +/- 1.3, mefenamic acid 13.6 +/- 0.6, bromosulphthalein 45 +/- 3, iopanoic acid approximately 200. Amiodarone and furosemide were inactive up to 100 microM. No displacement was observed with cortisol or the bile acid taurocholate, up to 100 microM. Dithiothreitol, 5 mM, did not change binding affinity or capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed2005

Fenamates and diltiazem modulate lipid-sensitive mechano-gated 2P domain K(+) channels.

A swelling-activated, background K(+) current in the corneal epithelium is characteristically activated by fenamates and inhibited by diltiazem. Fatty acids also stimulate this current, indicating that its origin is a lipid-sensitive mechano-gated 2P domain K(+) channel. In the present study, modulation of TREK-1, TREK-2, and TRAAK channels by fenamates and diltiazem was examined. TREK-1, TREK-2, and TRAAK currents transiently expressed in COS-7 cells were recorded by the perforated-patch configuration. As previously reported, arachidonic acid (20 microM) stimulated all of these channels, and a volatile anesthetic, halothane (1 mM) augmented TREK-1 and TREK-2 but not TRAAK. Flufenamic acid (FA, 100 microM), niflumic acid (NA, 100 microM), and mefenamic acid (MA, 100 microM) markedly stimulated TREK-1, TREK-2, and TRAAK. The potency sequence for the activation of TREK-1 and TREK-2 was FA > NA = MA, and the potency sequence for the activation of TRAAK was FA = NA > MA. Diltiazem (1 mM) inhibited TREK-1 and TREK-2, but not TRAAK. In conclusion, fenamates are openers of the lipid-sensitive mechano-gated 2P domain K(+) channels, and diltiazem may be a specific blocker for TREK. These novel findings could help to further understand channel functions of the mechano-gated 2P domain K(+) channels.

Animals↗
PubMed2004

The occurrence of selected human pharmaceutical compounds in UK estuaries.

This report describes a scoping study conducted in order to establish whether pharmaceutical compounds may be present in UK estuaries. Surface water samples collected from five UK estuaries were analysed for the presence of 14 pharmaceutical compounds selected from the priority lists of the UK Environment Agency and the Oslo and Paris Commission (OSPAR). The pharmaceutical compounds/metabolites clofibric acid, clotrimazole, dextropropoxyphene, diclofenac, ibuprofen, mefenamic acid, propranolol, tamoxifen and trimethoprim were detected at measurable concentrations in the samples collected. The concentrations of erythromycin, lofepramine, paracetamol, sulfamethoxazole and acetyl-sulfamethoxazole were all below the limits of detection of the methods used (between 4 and 20 ng l(-1)). The anti-fungal agent clotrimazole was the most frequently detected at a maximal concentration of 22 ng l(-1) and a median concentration of 7 ng l(-1). The analgesic compound ibuprofen was detected at a maximal concentration of approximately 930 ng l(-1) and a median concentration of 48 ng l(-1), whilst the other pharmaceutical compounds were detected between the limits of detection of the method used and 570 ng l(-1).

Ecosystem↗
PubMed2004

Determination of nonsteroidal anti-inflammatory drugs, caffeine, and triclosan in wastewater by gas chromatography-mass spectrometry.

Pharmaceuticals are a class of chemicals whose fate in the environment has received increasing attention in the past few years. A quantitative method was developed for the determination of acidic pharmaceuticals (ibuprofen, naproxen, ketoprofen, mefenamic acid, and diclofenac), caffeine and the antibacterial triclosan in wastewater effluent. The compounds were extracted from wastewater samples on Waters Oasis HLB solid-phase extraction columns, derivatized with N,O-bis [Trimethylsilyl] trifluoroacetamide (BSTFA) and analyzed using gas chromatography-mass spectrometry. Estimated method detection limits ranged from 6 to 45 ng/L based on replicate analyses (n = 10). This method was applied to the analysis of effluent from a wastewater treatment plant and compounds were detected at concentrations of 18-72 ng/L.

Anti-Infective Agents, Local↗
PubMed1976

Effect of anti-inflammatory agent on L-glutamine-D-fructose-6-phosphate transaminase.

The enzyme L-glutamineD-fructose-6-phosphate aminotransferase (EC 2.6.1.16) was isolated, partially characterized, and purified from the gastric mucosa of dogs. A new method, using 14C-fructose-6-phosphate, has been developed for the estimation of the enzyme activity. Several classes of standard anti-inflammatory agents including acetyl-salicylic acid, salicylic acid, flufenamic acid, phenyl-butazone, indometacin, mefenamic acid, oxyphenyl-butazone, antipyrine, aminophenazone, allopurinol, cortisol, and dimethylsulfoxide (DMSO) were found to be inhibitors of this enzyme. The property of inhibition of this amino-transferase could, thus, be used as a rapid in vitro test method for the primary screening of potential anti-inflammatory agents.

Animals↗
PubMed1985

In vivo anti-allergic and anti-inflammatory effects of drugs that inhibit lipoxygenase activity in vitro.

Studies in vitro have already shown that the chemotactic effect of leukotriene LTB4, as well as its pro-aggregatory effect on a suspension of leukocytes, could be inhibited by the lipoxygenase (LO) inhibitor ETYA; moreover a beneficial effect of another LO-inhibitor, diethylcarbamazine, has been shown on experimental asthma. To explore a possible therapeutic application of substances that inhibit 15-LO of soybean in vitro, we have tested several active compounds, namely nordihydroguaiaretic acid (NDGA), phenidone, diethylcarbamazine and mefenamic acid, on the following in vivo inflammation models in the rat: plantar oedema induced by carrageenin; cutaneous vascular hyperpermeability induced by pafacether; pleurisy induced by carrageenin. The correlation between the LO-inhibitor effect of these compounds in vitro and their beneficial effects in the different tests that were performed, as well as the mechanisms of action induced in the different experimental models, are discussed.

Animals↗
PubMed1996

Influence of non-steroidal anti-inflammatory drugs on the binding kinetics of dansylsarcosine to human serum albumin. Stereoselectivity, steric and inductive effects.

The effect of a series of non-steroidal anti-inflammatory drugs (NSAIDs) on the binding kinetics of dansylsarcosine (CAS 72517-44-3, DS), a marker ligand for the benzodiazepine binding site, and human serum albumin (HSA) was studied using the stopped-flow method. Both native (7% glycated) and 25% glycated HSA were used. The binding parameters were determined on the basis of the consecutive model. The DS association rate constant (k2) was 649 +/- 84 s-1 and 375 +/- 13 s-1 for 7% and 25% glycated HSA, respectively. These values were substantially influenced by addition of NSAIDs (molar ratio HSA:NSAID = 2:1), depending on the structure of NSAIDs. The calculated DS dissociation rate constant (k-2) was approximately 20 s-1. this value did not show marked dependence on the degree of glycation or on the presence of NSAIDs at the concentration used. The values were similar to estimates of kd (the displacement rate constant of DS) with the exception of diclofenac (CAS 15307-86-5) where kd was significantly lower, reaching 4.8 +/- 0.4 s-1 and 4.8 +/- 0.6 s-1 vs. k-2 parameters of 14 +/- 2.8 s-1 and 15 +/- 3.7 s-1 for 7% and 25% glycated HSA, respectively. A comparison of the enantiomers R- and S-ibuprofen (CAS 15687-27-1) and the regioisomers fenbufen (CAS 36330-85-5) and ketoprofen (CAS 22071-15-4) showed slight or no stereoslectivity of effects on the DS binding kinetics. However, the binding was influenced by bulk and nature of substituents at the aryl rest of propionic acid. The results obtained for mefenamic acid (CAS 61-68-7) suggest that this NSAID binds to a site of human serum albumin other than site II. Increased concentrations of glycoalbumin, as observed in diabetic patients, are not presumed to have inhibitory effects additional to that of NSAIDs which interact differentially with drugs at site II of HSA.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1990

Anti-oxidative profile of lobenzarit disodium (CCA).

The effects of lobenzarit disodium (CCA) on various species of activated oxygen were investigated in chemiluminescence experiments. CCA showed a quenching effect against hydroxyl radicals generated by Fenton reaction. The inhibition of CCA was much more intense than that of mefenamic acid which is an anti-inflammatory drug and an analogous compound to CCA. CCA also showed a quenching effect against singlet oxygen generated in enzymatic systems. However, CCA had no effect against superoxide anion radicals generated in the xanthine oxidase-hypoxanthine system. As a model of lipid peroxidation and protein alteration induced by activated oxygen, we examined the auto-oxidation of linolenic acid and the UV irradiation of immunoglobulin G (IgG). CCA inhibited the production of lipid peroxide; however CCA did not show a direct quenching action against lipid radicals which had been previously generated. CCA also inhibited the IgG alteration induced by UV irradiation. These results indicate that CCA has anti-oxidative actions with specificity for activated oxygen species and that CCA protects against lipid and protein damage induced by activated oxygen.

Antioxidants↗
PubMedDate not supplied

Deviation of the ratio of drugs in a two-component mixture encapsulated in cellulose phthalate microspheres.

Microspheres were formed when a solution of cellulose phthalate was extruded into 30% glacial acetic acid solution. Sulphonamides entrapped in such microspheres leached into the hardening solution because they dissolved freely in the acetic acid solution. This resulted in poor loading efficiency of the sulphonamides in the microspheres. When mixtures of sulphaguanidine and sulphathiazole in various drug ratios were microencapsulated by this method, the observed drug ratios were found to be markedly changed. This was attributed to the difference in solubility of the two sulphonamides in acid such that their extent of diffusion into the hardening solution was not similar. NSAIDS such as ibuprofen and mefenamic acid which are acidic and more hydrophobic in nature are less soluble in acetic acid. These drugs were retained better in the microspheres during the hardening process and the loading efficiency was consequently improved. In cases where mixture of the NSAIDS were encapsulated, the drug ratios showed little deviation from the theoretical values. This study shows that loading of the CAP microspheres is dependent on the solubility of the drugs in acetic acid. When more than one drug is required to be microencapsulated, the drug ratio may change if the drugs have different solubility in acetic acid.

Cellulose↗