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PubMed1990

Mediation of bradykinin-induced contraction in canine veins via thromboxane/prostaglandin endoperoxide receptor activation.

1. Canine jugular and femoral veins were studied to determine the possible importance of thromboxane (TXA2) and prostaglandin endoperoxides (prostaglandin H2, PGH2) in mediating bradykinin(BK)-induced contraction. 2. Isolated vein rings incubated in modified Krebs solution contracted to TXA2/PGH2 analogs SQ26655 and U44069 with potency of contraction exceeding that for BK. The potency ranking for both veins was SQ26655 greater than U44069 greater than BK greater than PGF2 alpha greater than TXB2 much greater than PGD2. 3. The cyclo-oxygenase inhibitors indomethacin (3 x 10(-7) M) and flufenamic acid (10(-5) M) reduced BK contractions without affecting those induced by noradrenaline (NA). 4. TXA2/PGH2 receptor antagonists SQ29548 (10(-8) M) and BM13177 (10(-6) M) strongly inhibited BK-induced tension. The action of antagonists was reversible with negligible influence on NA-elicited contraction. Selective removal of endothelium had no effect on BK-induced contraction or the action of the antagonists. 5. The thromboxane synthase inhibitors dazoxiben (10(-4) M) and CGS 12970 (10(-5) M) had no significant inhibitory effect on BK-induced tension. 6. These results suggest that in canine jugular and femoral vein, the action of BK is largely dependent upon stimulation of the cyclo-oxygenase pathway to produce PGH2 and possibly TXA2, which can activate a smooth muscle TXA2/PGH2 receptor to elicit vasoconstriction.

Animals↗
PubMed1988

A rapid and sensitive high-performance liquid chromatographic method for the determination of diclofenac sodium in serum and its use in pharmacokinetic studies.

A rapid, and sensitive high-performance liquid chromatographic method has been developed for the determination of diclofenac sodium in serum using flufenamic acid as the internal standard. Serum protein was precipitated with acetonitrile. The drugs were eluted from a 5 microns C-8 reversed-phase column at ambient temperature with a mobile phase consisting of acetonitrile-water (50:50% v/v) adjusted to pH 3.3 with glacial acetic acid, at a flow rate of 2 mL min-1 with UV detection at 280 nm. Each analysis required no longer than 10 min. Quantitation was achieved by the measurement of the peak-height ratio and the relative and absolute recoveries varied from 90 to 98%. Detection limits for diclofenac sodium in serum is 25 ng mL-1. Intraday coefficients of variation (CV) ranged from 2.47 to 4.61% and interday CVs from 3.52 to 7% at three different concentrations. Preliminary stability tests showed that diclofenac sodium is stable for at least 2 weeks in serum after freezing. The method is applied for the determination of the pharmacokinetic parameters of diclofenac after administration of two formulations (enteric-coated tablet and slow-release tablet), to a healthy male volunteer.

Adult↗
PubMed2002

Oxidation induces a Cl(-)-dependent cation conductance in human red blood cells.

Oxidative stress induces complex alterations of membrane proteins in red blood cells (RBCs) eventually leading to haemolysis. To study changes of membrane ion permeability induced by oxidative stress, whole-cell patch-clamp recordings and haemolysis experiments were performed in control and oxidised human RBCs. Control RBCs exhibited a small cation-selective whole-cell conductance (236 +/- 38 pS; n = 8) which was highly sensitive to the external Cl(-) concentration: replacement of NaCl in the bath by sodium gluconate induced an increase of this cation conductance by about 85 %. Exposing RBCs to t-butylhydroxyperoxide (1 mM for 10 min) induced a twofold increase in this cation conductance which was further stimulated after replacement of extracellular Cl(-) by gluconate, Br(-), I(-) or SCN(-). In addition, lowering the ionic strength of the bath solution by isosmotic substitution of NaCl by sorbitol activated the cation conductance. The Cl(-)-sensitive and oxidation-induced cation conductance was Ca(2+) permeable, exhibited a permselectivity of Cs(+) > K(+) > Na(+) = Li(+) >> NMDG(+), and was partially inhibited by amiloride (1 mM) and almost completely inhibited by GdCl(3) (150 microM), but was insensitive to TEA, BaCl(2), NPPB, flufenamic acid or quinidine. DIDS (100 microM) reversibly inhibited the activation of the cation conductance by removal of external Cl(-). Oxidation induced haemolysis in NaCl-bathed human RBCs. This haemolysis was attenuated by amiloride (1 mM) and inhibited by replacement of bath Na(+) by the impermeant cation NMDG(+). The Na(+)- and Ca(2+)-permeable conductance might be involved in haemolytic diseases induced by elevated oxidative stress, such as glucose-6-phosphate dehydrogenase deficiency.

Cations↗
PubMed2002

ATP release from human airway epithelial cells studied using a capillary cell culture system.

Epithelial release of adenosine triphosphate (ATP), an important autocrine and paracrine signalling molecule, is acutely mechanosensitive and therefore difficult to study. We describe here a novel preparation that minimizes mechanical and metabolic perturbations, and use it to examine ATP secretion by epithelial cells. The Calu-3 cell line derived from human airway sub-mucosal glands was cultured in a hollow fibre bioreactor on porous capillaries that were perfused by a re-circulating medium pump. Cells became polarized and cultures were stable for > 5 months, as evidenced by microscopy and lactate production (approximately 250 microg (10(8) cells)(-1) day(-1)). Elevating apical flow rate 5-fold increased ATP secretion from approximately 200 to 6618 fmol min(-1). Reducing apical osmolarity by 25-43 % also increased ATP secretion, which then declined spontaneously to a plateau rate that persisted as long as hypotonic perfusion was maintained. Release deactivated rapidly after shear and osmotic stresses were terminated, and was not associated with detectable cell lysis. Lowering apical [Ca(2+)] to increase connexin hemichannel permeability also stimulated ATP release and increased secretion during both hyposmotic and shear stress; however, the connexin 43 blocker flufenamic acid inhibited shear-induced ATP release only in low-Ca(2+) solution, and therefore another secretory pathway may operate with physiological (i.e. mM) calcium. Regardless of the mechanism, the present results quantify ATP responses to mechanical and osmotic stimuli and demonstrate the usefulness of capillary cultures for studying epithelial secretion.

Adenosine Triphosphate↗
PubMed2004

Transient receptor potential-like channels mediate metabotropic glutamate receptor EPSCs in rat dopamine neurones.

Transient receptor potential (TRP) channels form cationic channels activated by diverse factors including mechanical stimuli, changes in osmolarity, pH and temperature, as well as the exogenous irritant, capsaicin. Metabotropic glutamate receptors have also recently been linked to TRP channel activation in neurones of the substantia nigra, hippocampus and cerebellum, suggesting a novel role for such channels in synaptic communication via endogenous neurotransmitters. We tested this for dopamine neurones in rat brain slices by characterizing the current-voltage relationship and pharmacology of EPSCs mediated by group I metabotropic glutamate receptor subtype 1 (mGluR1). Slow inward currents (273 +/- 35 pA peak amplitude, 381 +/- 25 ms latency, holding potential (V(h)) =-73 mV) representing evoked mGluR1 EPSCs were isolated in the presence of antagonists of AMPA, NMDA, GABA(A), GABA(B), muscarinic and glycine receptors. CPCCOEt (100 microM), an mGluR1 antagonist, blocked the residual EPSC in all recordings. mGluR1-activated EPSCs reversed polarity near -10 mV, consistent with the involvement of a cationic channel. Extracellular application of the non-selective TRP channel blockers SKF 96365, flufenamic acid and ruthenium red caused reversible inhibition of mGluR1-activated EPSCs. These characteristics parallel those of mGluR1 activation with an agonist and indicate the involvement of a TRP-like channel in mGluR1-mediated EPSCs.

Animals↗
PubMed2004

Functional characterization of a Ca(2+)-activated non-selective cation channel in human atrial cardiomyocytes.

Cardiac arrhythmias, which occur in a wide variety of conditions where intracellular calcium is increased, have been attributed to the activation of a transient inward current (Iti). Iti is the result of three different [Ca]i-sensitive currents: the Na(+)-Ca2+ exchange current, a Ca(2+)-activated chloride current and a Ca(2+)-activated non-selective cationic current. Using the cell-free configuration of the patch-clamp technique, we have characterized the properties of a Ca(2+)-activated non-selective cation channel (NSC(Ca)) in freshly dissociated human atrial cardiomyocytes. In excised inside-out patches, the channel presented a linear I-V relationship with a conductance of 19 +/- 0.4 pS. It discriminated poorly among monovalent cations (Na+ and K+) and was slightly permeable to Ca2+ ions. The channel's open probability was increased by depolarization and a rise in internal calcium, for which the Kd for [Ca2+]i was 20.8 microM. Channel activity was reduced in the presence of 0.5 mM ATP or 10 microM glibenclamide on the cytoplasmic side to 22.1 +/- 16.8 and 28.5 +/- 8.6%, respectively, of control. It was also inhibited by 0.1 mM flufenamic acid. The channel shares several properties with TRPM4b and TRPM5, two members of the 'TRP melastatin' subfamily. In conclusion, the NSC(Ca) channel is a serious candidate to support the delayed after-depolarizations observed in [Ca2+] overload and thus may be implicated in the genesis of arrhythmias.

Adenosine Triphosphate↗
PubMed1986

Influence of mouse genotype on passive systemic anaphylaxis by immune complexes.

The influence of mouse genotype on passive systemic anaphylaxis (PSA) by immune complexes was studied. PSA was induced by using Brucella abortus endotoxin as the antigen and rabbit anti-Brucella endotoxin antisera. Experiments using syngeneic mice as well as mice congenic for H-2 showed that the H-2 haplotype influenced the sensitivity of mice to PSA. Among the H-2 haplotypes studied, H-2b was the most sensitive, followed by H-2k and H-2d. Experiments using passive transfer of serum as well as the complement inhibitors suramin and flufenamic acid indicated that variations in complement levels under control of H-2 may be responsible for the effects described. Cyproheptadine, a blocker of serotonin and histamine receptors, and imidazol-alpha-ketoglutarate, an inhibitor of thromboxane synthesis, inhibited PSA, indicating that platelet aggregation, possibly mediated by activated components of the complement cascade, is an important feature in the development of PSA reactions in this system. Differences between strains for protection by cyproheptadine and for the effect of complement inhibitors indicated a role of early components of the classical pathway in this model.

Anaphylaxis↗
PubMed2003

Evidence of a role for TRPC channels in VEGF-mediated increased vascular permeability in vivo.

Vascular endothelial growth factor (VEGF) increases vascular permeability by stimulating endothelial Ca(2+) influx. Here we provide evidence that links VEGF-mediated increased permeability and endothelial intracellular Ca(2+) concentration ([Ca(2+)](i)) with diacylglycerol (DAG)-mediated activation of the transient receptor potential channels (TRPCs). We used the Landis-Michel technique to measure changes in hydraulic conductivity (L(p)) and fluorescence photometry to quantify changes in endothelial [Ca(2+)](i) in individually perfused Rana mesenteric microvessels in vivo and transfected nonendothelial cells in vitro. The membrane-permeant DAG analog 1-oleoyl-2-acetyl-sn-glycerol (OAG, 100 microM), which is known to increase Ca(2+) influx through TRPCs, transiently increased L(p) 3.8 +/- 1.2-fold (from 1.6 +/- 0.8 to 9.8 +/- 2.7 x 10(-7) cm.s(-1).cmH(2)O(-1); P < 0.0001; n = 18). Protein kinase C inhibition by bisindolylmaleimide (1 microM) did not affect the OAG-induced increases in L(p). OAG also significantly increased microvascular endothelial [Ca(2+)](i) in vivo (n = 13; P < 0.0001), which again was not sensitive to protein kinase C inhibition. VEGF induced a transient increase in endothelial [Ca(2+)](i) in human embryonic kidney cells (HEK-293) that were cotransfected with VEGF receptor 2 and TRPC-6 but not with control, VEGF receptor 2, or TRPC-6 expression vector alone (P < 0.01; n = 9). Flufenamic acid, which has been shown to enhance activity of TRPC-6 but inhibit TRPC-3 and -7, enhanced the VEGF-mediated increase in L(p) in approximately half of the vessels tested but inhibited the response in the other half of the vessels. These data provide evidence consistent with the hypothesis that VEGF increases vascular permeability via DAG-mediated Ca(2+) entry through TRPCs. Although the exact identities of the TRPCs remain to be confirmed, TRPC-6 appears to be a likely candidate in approximately half of the vessels.

Animals↗
PubMed1996

Alpha-adrenoceptor activation of a chloride conductance in rat iris arterioles.

Changes in membrane potential associated with alpha-adrenoceptor-mediated contraction of rat iris arterioles after nerve stimulation (10 Hz, 1 s) have been measured with conventional intracellular recording techniques. Two different types of intracellular responses were recorded. Cells that show a depolarization are proposed to represent the arteriolar smooth muscle cells because the characteristics of the depolarization are correlated with those of the contraction. Cells that show no response or a small hyperpolarization in response to nerve stimulation are proposed to represent the endothelial cells of the arteriole. Both the depolarization and the contraction were abolished by tetrodotoxin (1 microM), benextramine (10 microM), and prazosin (0.1 mM), indicating that they result from nerve-mediated activation of alpha-adrenoceptors. A small but significant part of the contraction (30%) and the depolarization (11%) was nifedipine sensitive (10 microM). Caffeine (1 mM) abolished the contraction and reduced the depolarization by one-half. Reducing the external chloride concentration also abolished the contraction and reduced the depolarization by 90%. Flufenamic acid (250 mM) abolished both the contraction and the depolarization. It is suggested that, in iris arterioles, the activation of synaptic alpha-adrenoceptors leads to the release of intracellular calcium that activates both the chloride channels in the cell membrane leading to depolarization and the intracellular contractile apparatus leading to vasoconstriction.

Animals↗
PubMed2005

Bistable behavior originating in the axon of a crustacean motor neuron.

Both vertebrate and invertebrate motor neurons can display bistable behavior in which self-sustained tonic firing results from a brief excitatory stimulus. Induction of the bistability is usually dependent on activation of intrinsic conductances located in the somatodendritic area and is commonly sensitive to action of neuromodulators. We have observed bistable behavior in a neuromuscular preparation from the foregut of the crab Cancer borealis that consists of the gastric mill 4 (gm4) muscle and the nerve that innervates it, the dorsal gastric nerve (dgn). Nerve-evoked contractions of enhanced amplitude and long duration (>30 s) were induced by extracellular stimulation when the stimulus voltage was above a certain threshold. Intracellular and extracellular recordings showed that the large contractions were accompanied by persistent firing of the dorsal gastric (DG) motor neuron that innervates gm4. The persistent firing could be induced only by stimulating a specific region of the axon and could not be triggered by depolarizing the soma, even at current amplitudes that induced high-frequency firing of the neuron. The bistable behavior was abolished in low-Ca2+ saline or when nicardipine or flufenamic acid, blockers of L-type Ca2+ and Ca2+-activated nonselective cation currents, respectively, was applied to the axonal stimulation region of the dgn. Negative immunostaining for synapsin and synaptotagmin argued against the presence of synaptic/modulatory neuropil in the dgn. Collectively, our results suggest that bistable behavior in a motor neuron can originate in the axon and may not require the action of a locally released neuromodulator.

Action Potentials↗
PubMed2006

VEGF activates receptor-operated cation channels in human microvascular endothelial cells.

OBJECTIVE: Vascular endothelial growth factor (VEGF) exerts many of its effects by stimulating endothelial calcium influx, but little is known about channels mediating VEGF-induced cation entry. The aim of this study was to measure and characterize for the first time the VEGF-activated cation current in human microvascular endothelial cells (HMVECs). METHODS AND RESULTS: Whole-cell patch-clamp recordings were made from HMVECs. During applied voltage ramps, VEGF activated a current that reversed at 0 mV, was sensitive to gadolinium, and required extracellular cations. Noise analysis yielded a single-channel conductance of 27 pS. The current was not dependent on intracellular calcium stores, and was not blocked by inositol triphosphate (IP3) receptor or serine/threonine kinase inhibition but was partially inhibited by flufenamic acid. A similar current was activated by 1-oleoyl-2-acetyl-sn-glycerol (OAG), a membrane-permeant analog of diacylglycerol (DAG). To determine whether VEGF could activate recombinant ion channels with similar properties, we investigated the effect of VEGF on Chinese hamster ovary cells cotransfected with VEGFR2 and the canonical transient receptor potential (TRPC) channels, TRPC3 or TRPC6. VEGF induced a similar current to that described above in VEGFR2-TRPC3 and VEGFR2-TRPC6 cells but not in cells transfected with either cDNA alone. CONCLUSIONS: VEGF activates a receptor-operated cation current in HMVECs and OAG can activate directly a similar current in these cells. VEGF is also able to activate heterologously expressed TRPC3/6 channels through VEGFR2.

Animals↗
PubMed2006

Functional expression of the TRPM4 cationic current in ventricular cardiomyocytes from spontaneously hypertensive rats.

Cardiac hypertrophy is associated with electrophysiological modifications, including modification of action potential shape that can give rise to arrhythmias. We report here a higher detection of a calcium-activated nonselective cation current in cardiomyocytes of spontaneously hypertensive rats (SHRs), a model of hypertension and heart hypertrophy when compared with Wistar-Kyoto (WKY) rat, its normotensive equivalent. Freshly isolated cells from the left ventricles of 3- to 6-month-old WKY rats or SHRs were used for patch-clamp recordings. In inside-out patches, the channel presented a linear conductance of 25+/-0.5 pS, did not discriminate Na(+) over K(+), and was not permeable to Ca(2+). Open probability was increased by depolarization and a rise in [Ca(2+)](i) (dissociation constant=10+/-5.4 micromol/L) but reduced by 0.5 mmol/L [ATP](i), 10 micromol/L glibenclamide, or flufenamic acid (IC(50)=5.5+/-1.7 micromol/L). Thus, it owns the fingerprint of the TRPM4 current. Although rarely detected in WKY cardiomyocytes, the current was present in >50% of patches from SHR cardiomyocytes. Moreover, by performing RT-PCR from ventricular samples, we observed that TRPM4 mRNA detection was higher in SHRs than in WKY rats. We propose that a TRPM4 current is expressed in ventricular cardiomyocytes from SHRs. According to its properties, this channel may contribute to the transient inward current implicated in delayed-after-depolarizations observed during [Ca(2+)] overload of cardiomyocytes.

Animals↗
PubMed1987

A high performance liquid chromatography method for the analysis of total and free indomethacin in serum.

A simple rapid and sensitive HPLC technique for the analysis of total and free plasma indomethacin concentrations in neonates is described. The advantages of the technique are small sample volumes (50 microL) enabling the use of capillary samples, direct extraction, low limits of detection (20 ng/mL) and good precision (CV less than 7% between-batch). Indomethacin and the internal standard (flufenamic acid) eluted within 12 min and the peaks were unaffected by indomethacin metabolites or by a number of commonly used drugs. The technique is suitable for the investigation into the pharmacokinetics of total and free indomethacin, in neonates with patent ductus arteriosus, and could be used to define a therapeutic window for free indomethacin levels to enable therapeutic drug monitoring to occur in this condition.

Chromatography, High Pressure Liquid↗
PubMed1980

Direct stimulation of bone resorption by epidermal growth factor.

Epidermal growth factor, isolated from mouse submaxillary glands (mEGF) and human urine (hEGF; urogastrone), and fibroblast growth (FGF) have been tested for their effect on bone resorption by measuring the release of previously incorporated 45Ca from cultured fetal rat long bone shafts. mEGF produced significant but slow stimulation of bone resorption which was maximal at 30 ng/ml and was not blocked by indomethacin, flufenamic acid, or R0 20-5720, structurally unrelated inhibitors of prostaglandins synthesis. mEGF increased thymidine incorporation in long bones at 1 ng/ml, a concentration which did not stimulate resorption. hEGF at 3-30 ng/ml produced a more rapid stimulation of resorption, which was also unaffected by inhibition of prostaglandin cyclooxygenase. Neither mEGF nor hEGF increased the concentration of prostaglandin E in the medium after 5 days of culture. FGF failed to stimulate resorption at concentrations of up to 1000 ng/ml. We conclude the EGF, but not FGF, is a direct stimulator of bone resorption. In contrast to the previously reported findings in mouse calvaria, this stimulation is not dependent on prostaglandin synthesis. Since there is abundant hEGF in human urine, this factor could be responsible for the calcium-mobilizing activity recently found in human urine concentrates.

Animals↗
PubMed2006

Enzymatic properties of a member (AKR1C20) of the aldo-keto reductase family.

AKR1C20, a member of the aldo-keto reductase (AKR) superfamily, found by mouse genomic analysis, exhibits the highest sequence identity (89%) with mouse liver 17beta-hydroxysteroid dehydrogenase (HSD) type 5, but its function remains unknown. In this report, we have expressed the recombinant AKR1C20 from its cDNA, and examined its properties. The purified enzyme was a 36-kDa monomer, and showed both 17beta-HSD and 3alpha-HSD activities in the presence of NADP(H) as the coenzymes. While the Km values for testosterone and 5alpha-dihydrotestosterone were high (>0.2 mM), those for 3alpha-hydroxy- and 3-keto-steroids were low (0.3-5 microM), resulting in high catalytic efficiency for the substrates. Although no significant dehydrogenase activity towards non-steroidal alcohols was observed, the enzyme highly reduced alpha-dicarbonyl compounds such as 16-ketoestrone, 9,10-phenanthrenequinone, acenaphthenequinone, 1-phenylisatin and camphorquinone. The pH optima of the dehydrogenase and reductase activities were 10.5 and 6.5-7.5, respectively. The enzyme was inhibited by sulfobromophthalein, hexestrol, indomethacin and flufenamic acid. The properties of AKR1C20 are distinct from those of previously known mouse 17beta-HSD type 5 (AKR1C6), 3alpha-HSD (AKR1C14) and other members of the AKR1C subfamily. Thus, AKR1C20 is a novel 3alpha(17beta)-HSD, which may also function as a reductase for xenobiotic alpha-dicarbonyl compounds.

17-Hydroxysteroid Dehydrogenases↗
PubMed1981

Stabilizing action of disodium cromoglycate on erythrocyte membrane.

Effect of disodium cromoglycate (DSCG) on hemolysis of rat erythrocytes was studied. The heat-induced hemolysis was remarkably inhibited by DSCG. This effect was not affected by normal rat serum and was maintained for longer than 60 min similar to the activity in clinical use, although the inhibitory effect of DSCG on reagin-induced histamine release from mast cell disappeared rapidly in 5 min after administration. Non-steroidal anti-inflammatory drugs such as flufenamic acid or phenylbutazone which are known to inhibit the hemolysis depending on their protein stabilizing activities inhibited both of the heat-induced hemolysis and albumin denaturation, but DSCG did not inhibit the albumin denaturation. Furthermore, it was also observed that DSCG inhibited the hemolysis induced by lipophilic agents such as saponin, linoleic acid or phospholipase C. These findings suggest that DSCG has a certain membrane stabilizing activity, in addition to the inhibitory effect on reagin-induced histamine release, and that the activity may be probably related to membrane lipids rather than membrane-proteins.

Animals↗
PubMed1985

[Anti-inflammatory activity of the dry distillation tar of delipidated soybean (Glyteer) (1)].

The anti-inflammatory activity of the dry distillation tar of delipidated soybean (GL, 0.1 approximately 10%) was investigated by its topical application to mice, rats and guinea pigs; and the effects were compared with those of betamethasone 17-valerate (BV, 0.12%), ibuprofen (IP, 5%), phenylbutazone (PB, 5%) and flufenamic acid (FA, 5%), which were all prepared with the same ointment base. GL (1 approximately 10%) showed a concentration-dependent inhibition of the increased vascular permeability induced by histamine and bradykinin in guinea pigs. GL significantly inhibited rat paw edema induced by carrageenin, but in serotonin-induced paw edema, GL showed only a weak effect. GL also inhibited the erythema formation induced by ultra-violet rays, and the activity was equal to that of PB. The inhibitory potency of GL against the erythema formation induced by arachidonic acid in guinea pigs was equal to that of IP. It is suggested from these results that the mode of action of GL is similar to that of other acidic non-steroidal anti-inflammatory drugs. However, GL did not inhibit paper disk granuloma in rats. Furthermore, GL markedly inhibited the delayed-type hypersensitivity induced by picryl chloride, and the activity was stronger than that of IB, PB and FA. Here GL showed the mode of action seen with steroidal anti-inflammatory drugs. The present data provide evidence that GL applied externally possesses a potent effect as an anti-inflammatory drug.

Administration, Topical↗
PubMed1988

[Anti-inflammatory activity of the dry distillation tar of delipidated soybean (Glyteer) (2)].

The anti-inflammatory effects of Glyteer (GL) were investigated by its local administration using the CMC-pouch method in rats, and the effects were compared with those of betamethasone 17-valerate (BV, 1 mg), phenylbutazone (PB, 10 mg), flufenamic acid (FA, 10 mg), bufexamac (BM, 10 and 20 mg), bendazac (BZ, 10 and 20 mg), icthammol (IT, 10 mg) and pine tar (PT, 10 mg). At three hours after CMC-treatment, GL (10 mg) significantly inhibited not only the protein exudation, but also the leucocyte migration. The inhibitory activity of GL on the leucocyte migration had the same potency as that of FA, but was stronger than those of PB, BV, BM, BZ, IT and PT. Furthermore, in relation to the leucocyte migration, GL markedly inhibited not only the neutrophil, but also the macrophage migration. At three hours after CMC-treatment, the inhibitory activity of GL on the neutrophil migration had the same potency as those of PB and FA, but was stronger than those of BV, BM, BZ, IT and PT. On the other hand, GL, BM, BZ, FA, IT and PT had an inhibitory activity on the macrophage migration, and the activity was more potent in GL, FA and IT. From these results, it is suggested that the inhibition of GL on increased vascular permeability and leucocyte migration is one of the mechanisms of its anti-inflammatory action.

Administration, Topical↗