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S Oga

Publications and source records attributed to S Oga.

At least 19 recordsLinked to original sources
PubMed2004

Anti-inflammatory, antinociceptive and ulcerogenic activity of a zinc-diclofenac complex in rats.

We investigated the anti-inflammatory, antinociceptive and ulcerogenic activity of a zinc-diclofenac complex (5.5 or 11 mg/kg) in male Wistar rats (180-300 g, N = 6) and compared it to free diclofenac (5 or 10 mg/kg) and to the combination of diclofenac (5 or 10 mg/kg) and zinc acetate (1.68 or 3.5 mg/kg). The carrageenin-induced paw edema and the cotton pellet-induced granulomatous tissue formation models were used to assess the anti-inflammatory activity, and the Hargreaves model of thermal hyperalgesia was used to assess the antinociceptive activity. To investigate the effect of orally or intraperitoneally (ip) administered drugs on cold-induced gastric lesions, single doses were administered before exposing the animals to a freezer (-18 degrees C) for 45 min in individual cages. We also evaluated the gastric lesions induced by multiple doses of the drugs. Diclofenac plus zinc complex had the same anti-inflammatory and antinociceptive effects as diclofenac alone. Gastric lesions induced by a single dose administered per os and ip were reduced in the group treated with zinc-diclofenac when compared to the groups treated with free diclofenac or diclofenac plus zinc acetate. In the multiple dose treatment, the complex induced a lower number of the most severe lesions when compared to free diclofenac and diclofenac plus zinc acetate. In conclusion, the present study demonstrates that the zinc-diclofenac complex may represent an important therapeutic alternative for the treatment of rheumatic and inflammatory conditions, as its use may be associated with a reduced incidence of gastric lesions.

Analgesics↗
PubMed2000

Acute and subacute toxicity of Cochlospermum regium (Mart. & Schr.) pilger.

The toxicity of a hydroethanol extract of the subterranean part of Cochlospermum regium was evaluated in mice and rats. The extract had moderate acute toxicity when administered intraperitoneally and low toxicity upon oral administration. A subacute toxicity test revealed that the extract is well tolerated by these animals.

Administration, Oral↗
PubMed2000

Effect of Maytenus aquifolium extract on the pharmacokinetic and antiinflammatory effectiveness of piroxicam in rats.

This study explored the interference by Maytenus aquifolium leaves hydroalcoholic (MALHE) extract, administered orally, on the pharmacokinetic and antiinflammatory activity of piroxicam in rats. The results showed no significant difference in piroxicam bioavailability with simultaneous application of MALHE. MALHE also had no effect on the inhibitory effect of piroxicam on inflammatory processes induced by carrageenan and complete Freund adjuvant.

Animals↗
PubMed2000

Clinical and laboratory parameters in dapsone acute intoxication.

OBJECTIVE: To determine the severity of dapsone (DDS) acute intoxication - an uncommon medical event - using clinical and laboratory parameters. METHODS: Two hundred and seventy four patients with acute DDS intoxication, aged 1 month to 50 years old, were studied and classified into four age groups. Clinical evaluation was assessed through a protocol and correlated with laboratory parameters. Spectrophotometric methods were used to analyze methemoglobinemia (MHbp) and dapsonemia (DDSp). RESULTS: The most prevalent clinical sign of intoxication was cyanosis, seen in 65.7% of the patients and in 100% of children less than 5 years of age. According to laboratory criteria, MHbp-related severe clinical intoxication was seen in 56.2% and DDSp-related occurred in 58% of the patients. Regarding DDSp, intoxication was considered severe when 20 tablets (100 mg each) were ingested, a median of 29 microg/ml. Regarding MHbp, intoxication was severe when 7.5 tablets were ingested, a median of 38% of the total Hb. The correlation between MHbp and DDSp was statistically significant (n=144, r=0.32, p<0.05). Negative correlation was observed between MHbp and the time elapsed since DDS intake (n=124, r=-0.34, p<0.001). There was also a negative correlation between DDSp and the time elapsed since DDS intake (n=63, r=-0.35, p<0.0001). CONCLUSIONS: Longitudinal analysis showed a significant association between methemoglobinemia and the time elapsed after the intake (t), according to the equation: Dapsonemia = 12.9256 - 0.0682t + 0.234 methemoglobinemia

Adolescent↗
PubMed1999

Börjeson-Forssman-Lehmann syndrome in a woman with skewed X-chromosome inactivation.

Börjeson-Forssman-Lehmann (BFL) syndrome is an X-linked recessive disorder characterized by minor facial anomalies, obesity, epilepsy, and severe mental retardation. The phenotype of male patients is usually severe, whereas that of carriers is less severe, suggesting X-linked incompletely recessive inheritance. A recent linkage study mapped the BFL syndrome gene to Xq26-q27. The etiology of the condition in female patients with full manifestations is not known, although nonrandom X-chromosome inactivation has been considered. We recently developed an assay for X-inactivation studies based on the methylation-specific polymerase chain reaction (PCR) technique. Using the methylation-specific PCR assay, a woman with typical findings of this syndrome was shown to have an extremely skewed X-inactivation pattern. This finding suggests that the full manifestations of the BFL syndrome in carriers may be caused by skewed X inactivation with a high proportion of cells in which the X chromosome with a normal gene be inactivated, leaving the X chromosome with a mutant gene active.

Adult↗
PubMed1999

Increased activity of membrane glycoprotein PC-1 in the fibroblasts from non-insulin-dependent diabetes mellitus patients with insulin resistance.

Although most of patients with non-insulin-dependent diabetes mellitus (NIDDM) have insulin resistance, it is unknown whether a molecule might interfere with insulin action. Membrane glycoprotein PC-1 (plasma cell antigen-1), which inhibits insulin receptor tyrosine kinase activity, was isolated from fibroblasts of NIDDM patients. Because PC-1 content in skeletal muscle and adipose tissue correlated with whole body insulin sensitivity, PC-1 might play a role in insulin resistance. In order to know whether PC-1 activity of fibroblasts is also elevated in Japanese NIDDM patients, and whether PC-1 activity correlates with the parameters of insulin resistance in vivo or not, we measured PC-1 activity of cultured fibroblasts from 17 patients with NIDDM and seven healthy controls. PC-1 activity of the NIDDM patients was 85.2 +/- 33.1 nmol/mg per min (mean +/- S.D.), and was higher than that of healthy controls (42.6 +/- 12.7 nmol/mg per min, P = 0.0002). Insulin sensitivity was measured in 11 of 17 NIDDM patients by the artificial pancreas. PC-1 activity of the patients with insulin resistance (glucose infusion rate < 3.0 mg/kg per min, n = 7) was elevated to 99.9 +/- 31.9 nmol/mg per min, while that of the other patients (n = 4) was 55.3 +/- 7.5 nmol/mg per min (P = 0.003). In conclusion, glycoprotein PC-1 activity of dermal fibroblasts is correlated with insulin resistance in patients with NIDDM.

Adult↗
PubMed1999

Pharmacokinetic profile and adverse gastric effect of zinc-piroxicam in rats.

Complexation of piroxicam with zinc extends its absorption time in rats. The time of peak concentration value for complexed piroxicam was 5.27 hr compared to only 2.56 hr for the uncomplexed agent. Piroxicam and zinc-piroxicam show similar inhibitory effects on carrageenin-induced paw edema. Zinc-piroxicam is less irritating than piroxicam on the gastric mucosa.

Aminocaproates↗
PubMed1997

Pharmacokinetic profile of piroxicam beta-cyclodextrin, in rat plasma and lymph.

1. The absorption of piroxicam into the blood of rats is significantly slower after oral administration of piroxicam beta-cyclodextrin than of free piroxicam. 2. The pharmacokinetic profiles of piroxicam in rat lymph were very similar in both groups. 3. Bioavailability of piroxicam in plasma is higher after treatment with the inclusion product than with free piroxicam. On the other hand, bioavailability in lymph is higher when free piroxicam is administered.

Animals↗
PubMed1995

Effect of piroxicam beta-cyclodextrin complex on experimental inflammation.

1. The effectiveness of the inclusion product of piroxicam with beta-cyclodextrin was compared to that of free piroxicam on inflammatory reactions by using three experimental inflammatory models in rats. 2. The inclusion compound showed anti-inflammatory effects similar to those of simple piroxicam on granuloma tissue formation and arthritis induced by complete Freund adjuvant. 3. In carrageenin-induced pleurisy, the piroxicam beta-cyclodextrin reduced leukocyte mobilization more intensely than non-complexed piroxicam. 4. These results suggest that beta-cyclodextrin is a useful tool for improving the efficacy of piroxicam.

Animals↗
PubMed1994

Hyperalgesia induced by Bothrops jararaca venom in rats: role of eicosanoids and platelet activating factor (PAF).

In this study we investigated the ability of Bothrops jararaca venom (BjV) to induce hyperalgesia and the modulation of this effect by lipid mediators. It was found that intraplantar injection of BjV (1 to 25 micrograms) caused a dose and time-related hyperalgesia. The peak of the hyperalgesic response was 1 hr after injection of the venom and persisted for 24 hr with the higher dose. The BjV-induced hyperalgesia was markedly attenuated by dexamethasone. Dexamethasone blocks the generation of biologically active metabolites from arachidonic acid by inhibiting PLA2 activation. Inhibition of the cyclo-oxygenase pathway by indomethacin, or inhibition of lipoxygenases by NDGA both significantly inhibited BjV-induced hyperalgesia. Two antagonists of PAF, WEB2170 and BN52021, also significantly inhibited the initial phase of the hyperalgesia. These results suggest that hyperalgesia induced by BjV is, at least partially, mediated by lipid mediators such as prostaglandins, leukotrienes and PAF.

Animals↗
PubMed1991

Synthesis, characterization, and biological screening of a copper flurbiprofen complex with anti-inflammatory effects.

The flurbiprofen complex of copper(II) was prepared and characterized by IR, UV-VIS and EPR Spectroscopy, magnetic susceptibility, and thermogravimetric analysis. The compound was tested for in vivo anti-inflammatory and analgesic activities in rats. The inhibitory effect on carrageenin-induced paws inflammation and analgesic effect of copper flurbiprofen complex were similar to those of free flurbiprofen. However, the copper complex produced less gastric irritation than the parent drug.

Analysis of Variance↗
PubMed1991

Histamine release from rat mast cells induced by econazole.

1. Econazole released histamine from rat mast cells in vitro. This response was not affected by the addition of calcium or by prior treatment of mast cells with EDTA or cromoglycate. 2. Rat mast cells treated with econazole were stained by the vital dye trypan blue. 3. The intradermal injection of econazole increased vascular permeability. This response was antagonized by chlorpheniramine and cyproheptadine. 4. Our results demonstrate that econazole releases histamine by the "nonselective" mechanism. It is suggested that econazole inflammatory effects may be due to histamine release from mast cells.

Animals↗
PubMed1990

Inhibitory effects of beryllium chloride on rat liver microsomal enzymes.

A single i.v. dose (0.1 mmol Be2+/kg) of beryllium chloride prolonged the duration of pentobarbital-induced sleep and zoxazolamine-induced paralysis, in rats. The effects are correlated with changes of the pharmacokinetic parameters and with the in vitro inhibition of both aliphatic and aromatic hydroxylation of pentobarbital and zoxazolamine. In vitro N-demethylation of meperidine and aminopyrine was partially inhibited while O-demethylation of quinidine was unaffected by liver microsomes of rats pretreated with beryllium salt. The findings give clues that beryllium chloride inhibits some forms of cytochrome P-450, especially those responsible for hydroxylation of substrates, like pentobarbital and zoxazolamine.

Animals↗
PubMed1990

Propylene glycol enhances anti-inflammatory effects of phenylbutazone.

1. The interference of propylene glycol with anti-inflammatory effects of phenylbutazone was investigated. 2. Inhibitory effect of phenylbutazone on both carrageenin-induced edema and the cotton pellet granuloma was increased when propylene glycol was used as solvent. 3. Propylene glycol given alone inhibited carrageenin-induced edema and pleurisy, as well as granulomatous tissue formation. 4. Some pharmacokinetic parameters of phenylbutazone were also changed by propylene glycol administered simultaneously. 5. These results suggest that propylene glycol probably increases the anti-inflammatory effect of phenylbutazone by summation and by raising the plasma half-life and the distribution volume of phenylbutazone.

Adrenalectomy↗
PubMed1986

Effect of praseodymium chloride on liver microsomal enzymes of rats.

A single i.v. dose (5 mg/kg) of a light lanthanon, praseodymium, prolonged the duration of hexobarbital-induced sleep and zoxazolamine-induced paralysis, as well as it modified pharmacokinetic parameters of hexobarbital and zoxazolamine, in rats. Half-lives (t1/2) and area under the curve (AUC) were increased, while elimination coefficient (beta) and clearance (Cl) were decreased. However, in daily doses of 1 mg/kg i.p. for 15 days, praseodymium did not alter pharmacological effects and pharmacokinetic parameters. The in vitro hydroxylation of hexobarbital and zoxazolamine by liver microsomes was inhibited when the animals were treated previously with a single i.v. dose (5 mg/kg) of praseodymium chloride. In these animals, the amount of cytochromes P-450 and b5 were reduced significantly, whereas that of NADPH-cytochrome c reductase remained unchanged. The pretreatment of animals with phenobarbital normalized the microsomal enzyme impairment caused by praseodymium.

Animals↗
PubMed1985

Some characteristics of econazole-induced pleurisy in rats.

Aqueous suspension of econazole nitrate injected into the pleural cavity of rats induces sharp exudate formation and small leucocyte mobilization. The econazole pleurisy development is monophasic and its peak value occurs between 8 and 12 hr after econazole injection. The exudate volume and the leucocyte mobilization are inhibited by chlorpheniramine, cyproheptadine and steroidal and non-steroidal anti-inflammatory drugs.

Animals↗