PubMed Health⌕ Search

Biomedical subjects

K Ohuchi

Publications and source records attributed to K Ohuchi.

At least 145 records · Page 8Linked to original sources
PubMed1984

Arachidonate metabolites in acute and chronic allergic air pouch inflammation in rats and the anti-inflammatory effects of indomethacin and dexamethasone.

Two types of allergic air pouch inflammation, the acute and the chronic types, were induced in the dorsum of rats. 1, 8, and 24 h after the immunologic challenge injection, the exudate contents of cyclooxygenase products, prostaglandin (PG)E2, 13,14-dihydro-15-keto-PGE2, PGI2 (measured as 6-keto-PGF1 alpha) and PGD2, and the lipoxygenase products, hydroxyeicosatetraenoic acids (HETEs) and 6-sulfido-peptide-containing leukotrienes (SRS) were measured by radioimmunoassay. The effects of locally injected indomethacin or dexamethasone on the exudate volumes and the number of cells in the exudates in both types of allergic inflammation and the effects of these drugs on the contents of the cyclooxygenase and lipoxygenase products in the exudates 8 h after the challenge injection were examined.

Animals↗
PubMed1983

Inhibition by AA861 of prostaglandin E2 production by activated peritoneal macrophages of rat.

Prostaglandin E2 production by rat peritoneal activated macrophages was inhibited by AA861 which had been reported as a selective inhibitor of 5-lipoxygenase from guinea pig peritoneal leukocytes. At a dose of 3.06 microM, prostaglandin E2 production was decreased to 27% of control. No inhibition of the release of (3H)arachidonic acid from the prelabeled macrophages was observed at the dose.

Animals↗
PubMed1983

Slow reacting substance in the exudate of allergic air pouch inflammation in rats.

The activity of slow reacting substance was examined in the exudate of the allergic inflammation in rats after partial purification by alkaline decomposition and XAD-8 anion-exchange column chromatography. The guinea-pig ileum contractile substance from the exudate collected at 1 hr after the challenge injection was attributed to leukotriene (LT) C4 and/or D4 since the activity was selectively antagonized by FPL 55712. Participations of histamine, acetylcholine and prostaglandin E2 were ruled out. However, the contraction pattern due to the partially purified substance collected at 24 hr after the challenge injection was different from that at 1 hr. The guinea-pig ileum was contracted much more slowly than by synthetic LT C4 or D4 and this contraction was not antagonized by FPL 55712. It was demonstrated that some unidentified materials exist in the exudate of the allergic air pouch inflammation which contract isolated guinea-pig ileum in a different manner from synthetic LT C4 or D4.

Air↗
PubMed1983

Correlation of leukocyte accumulation with chemotactic activity in the exudate of an allergic air-pouch inflammation.

Chemotactic activity at the site of an allergic air-pouch inflammation induced with azobenzene-arsonate-conjugated acetyl bovine serum albumin as an antigen was studied and a close correlation of the chemotactic activity with the intensity of leukocyte migration was demonstrated. In the period of vigorous leukocyte immigration into the fluid in the allergic air-pouch, chemotactic activity of the exudate was maintained at a high level, while no significant activity was detected after the number of leukocytes in the pouch fluid reached maximum.

Animals↗
PubMed1982

Phospholipase A2 activity in carrageenin-induced inflammatory tissue of rats.

Phospholipase A2 activity was detected in 7-day-old carrageenin-induced inflammatory tissue of rats using a synthetic substrate. 1-acyl-2-[3H]arachidonyl-phosphatidylcholine. The inflammatory tissue was homogenized in saline containing 1 M KCl, and the 105,000 g supernatant fraction was placed on a Sephadex G-100 column. The partially purified phospholipase A2 had a pH optimum at 6-7 and was Ca2+ dependent. p-Bromophenacyl bromide was strongly inhibitory to the partially purified phospholipase A2 (IC50 = 1.44 x 10(-5) M). A moderate inhibition was observed with indomethacin. Cycloheximide and dexamethasone, which inhibit prostaglandin production in inflammatory tissue, exerted no direct inhibitory action on the phospholipase A2. There were no direct inhibitory effects of quinacrine, bradykinin, or actinomycin D. The cell-free supernatant fraction of the inflammatory exudate of 7-day-old carrageenin-induced granulation tissue was found to have no phospholipase A2 activity.

Animals↗
PubMed1982

Mechanism of inhibitory action of mesaconitine in acute inflammations.

Mesaconitine (MA) inhibited carrageenin-induced hind-paw edema in sham-operated mice as well as adrenalectomized mice. Hind-paw edema produced by subplantar injection of histamine, serotonin and prostaglandin E1 was suppressed by MA, indicating that it elicits the antiinflammatory activity at the early exudative stage of inflammations. However, MA did not affect the biosynthesis of the prostaglandins. Trazoline and propranolol had no effect on the inhibitory activity of MA on carrageenin-induced hind-paw edema. MA when administered i.c. at the doses where it shows marked analgesic activity produced dose-dependent antiinflammatory responses on paw edema produced by carrageenin and on vascular permeability accelerated by acetic acid and agar. The inhibitory activity of morphine on carrageenin-induced paw edema failed to be potentiated by the concurrent administration of MA, demonstrating that the mechanism of the antiinflammatory activity of MA involves the central nervous system.

Aconitine↗
PubMed1982

A possible role of arachidonate metabolism in allergic air pouch inflammation in rats. Anti-inflammatory effect of indomethacin and dexamethasone and the level of prostaglandin E2 in the exudate.

The effect of indomethacin and dexamethasone on an allergic inflammation in rats, a novel model of allergic inflammation of an air pouch type, was examined. Indomethacin and dexamethasone exerted a dose-dependent inhibition of both the accumulation of inflammatory exudate and the migration of leukocytes into the exudate. And although prostaglandin E2 levels in the exudate were lowered to the same extent by treatment with indomethacin and dexamethasone, inhibition of both exudate accumulation and and leukocyte migration was more pronounced after treatment with dexamethasone. The difference in the effectiveness of indomethacin and dexamethasone in terms of inhibition of arachidonate metabolism in the allergic air pouch inflammation are discussed.

Animals↗
PubMed1982

Induction of an allergic air-pouch inflammation in rats.

An allergic air pouch inflammation was induced on the dorsum of rats using azobenzenearsonate-conjugated acetyl bovine serum albumin as an antigen. Rats were immunized by intradermal injection with 5 mg of the antigen in 0.5 ml Freund's complete adjuvant saline (1:1) emulsion. 9 days after the immunization 8 ml of air was injected subcutaneously on the dorsum, and 24 h later 4 ml of 2% sodium carboxymethyl cellulose solution containing 2 mg of the antigen was injected into the preformed air pouch to provoke the allergic inflammation. In addition to the histological observations of the inflammatory tissues of the pouch wall, time course studies on the volume of the inflammatory pouch fluid, on the number and species of inflammatory cells in the pouch fluid and on the wet weight of granulation tissues were carried out to characterize the nature of the inflammatory reaction, which was shown to be suitable as a model to perform quantitative measurements and biochemical analyses of the allergic inflammation.

Animals↗
PubMed1982

Induction of a delayed type hypersensitivity to carrageenin in mice.

Induction of delayed type hypersensitivity to carrageenin in mice was investigated with successful results. Male ddY/s mice were immunized with 1 mg of carrageenin 100 microliters of Freund's complete adjuvant-saline (1:1) emulsion and challenged 10 d after the immunization on their footpads with either 10 or 40 micrograms of the antigen in 2.5 microliters of Freund's incomplete adjuvant-saline (1:1) emulsion. The mice exhibited a strong allergic footpad reaction at 24-48 h after the challenge injection. The footpad reaction was successfully transferred with spleen cells. Non-steroidal antiinflammatory drug, indomethacin, and steroidal antiinflammatory drug, dexamethasone, suppressed the delayed type hypersensitivity reaction.

Animals↗
PubMed1981

Suppression by dexamethasone of vascular permeability responses induced with leukotrienes C and D in the rat skin.

The present experiment was designed to investigate whether glucocorticoids counteract proinflammatory action of leukotrienes C and D which were suggested to play an important role as mediators in the inflammatory exudate response. Vascular permeability was measured using 131I-labeled human serum albumin (131I-HSA) as a tracer. The vascular permeability was elevated promptly after intradermal injection of chemically synthesized leukotriene C or D and then rapidly fell down to the control level. A positive dose-response relationship was observed in the dose levels of 0.01-1 microgram of leukotrienes. Dexamethasone at doses of 0.15, 0.5 and 1.5 mg/kg caused dose-dependent suppression of vascular permeability response induced with leukotrienes C and D. The present data indicate that glucocorticoids are capable of exerting direct inhibitory effect against proinflammatory action of leukotrienes C and D produced through phospholipase A2-arachidonate-lipoxygenase pathway.

Animals↗
PubMed1981

Glycyrrhizin inhibits prostaglandin E2 production by activated peritoneal macrophages from rats.

Glycyrrhizin was found to inhibit prostaglandin E2 production by activated rat peritoneal macrophages. Preincubation of the cells with glycyrrhizin increases its inhibitory effectiveness. Glycyrrhetinic acid, the aglycone of glycyrrhizin, at a dose of 100 microgram per ml also inhibited prostaglandin E2 production, but the inhibition was considered to be attributable to a toxic effect on the cells since more than 30% of the cells were detached from the dish during the 8 hr incubation period. In contrast, glycyrrhizin did not detach the cells from the dish at doses up to 3 mg per ml. Release of [3H]arachidonic acid from prelabeled cells was also inhibited by glycyrrhizin. It is likely that anti-inflammatory activity of glycyrrhizin depends at least in part on its inhibitory effect of the production of prostaglandin E2.

Animals↗
PubMed1981

Change of prostaglandin E level in joint fluids after treatment with flurbiprofen in patients with rheumatoid arthritis and osteoarthritis.

The prostaglandin E (PGE) level in the knee joint fluid was determined by radioimmunoassay before and after anti-inflammatory therapy with flurbiprofen in 8 patients with rheumatoid arthritis (RA) and 4 patients with osteoarthritis (OA). The level of PGE in RA joint fluids before the anti-inflammatory treatment was 9.5-1.2 ng/ml and in proportion with the leucocyte count in the joint fluid. A marked decrease of the PGE level was attained with flurbiprofen treatment in 4 patients whose initial PGE levels had been higher than 3.2 ng/ml, while 4 patients with lower PGE levels, namely, 1.4-1.2 ng/ml, did not respond to the drug treatment. In all the OA patients the PGE levels was no higher than 1.5 ng/ml and refractory to the anti-inflammatory therapy.

Adult↗
PubMed1981

Delayed-type hypersensitivity as revealed on the footpads of mice to azobenzenearsonate-acetyl bovine serum albumin.

A strong delayed-type footpad reaction was established in mice using azobenzenearsonate-acetyl bovine serum albumin (ABA-AcBSA) as an antigen. Male ddY/S mice were sensitized by subcutaneous injection of 100 microliter of Freund's complete adjuvant - saline (1:1) emulsion containing 100 microgram of the antigen and challenged by subcutaneous injection of 2.5 microliter of Freund's incomplete adjuvant - saline (1:1) emulsion with 2.5 microgram antigen in the footpad on the 10th day after the sensitization. The analysis of the system which fulfilled criteria for delayed-type hypersensitivity with regard to kinetics, passive transfer and histology of the footpad reaction, and the effect of dexamethasone, indomethacin and quinacrine on the footpad reaction were described.

Animals↗
PubMed1980

alpha-Tocopherol inhibits 12-O-tetradecanoyl-phorbol-13-acetate-stimulated deacylation of cellular lipids, prostaglandin production, and changes in cell morphology of Madin-Darby canine kidney cells.

Incubation of the tumor-promoting phorbol diester, 12-O-tetradecanoyl-phorbol-13-acetate with Madin-Darby canine kidney cells (MDCK) stimulated deacylation of phospholipids, prostaglandin production and altered cell morphology. alpha-Tocopherol, if present during the incubation, inhibited these effects. For inhibition, alpha-tocopherol had to be present during incubation of 12-O-tetradecanoyl-phorbol-13-acetate and cells; pretreatment or posttreatment of the cells with alpha-tocopherol was not effective. Inhibition of the 12-O-tetradecanoyl-phorbol-13-acetate effects was specific for the tumor promoter extracted from the Croton tiglium L. plant of the family Euphorbiaceae. Stimulated prostaglandin production by another tumor promotor (phorbol-12, 13-didecanoate), a semisynthetic product of that plant, was also inhibited by alpha-tocopherol. But that of structurally related diterpenoid esters isolated from plants of the family Thymelaeaceae, such as mezerein, gnidimacrin, gnilatimacrin, and gnilatimacrin-20-palmitate, were not. Stimulation of prostaglandin production in MDCK cells by compounds such as benzo(a)pyrene, adriamycin and 17 beta-estradiol or even the basal synthetic activity of MDCK cells was not affected by alpha-tocopherol.

Animals↗
PubMed1980

Prostaglandin production by minced carrageenin granuloma tissue of rats and its inhibition by dexamethasone and cycloheximide.

Seven-day-old carrageenin granuloma tissue of rats, when incubated in organ culture, produced 6-keto-prostaglandin F1 alpha, prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in ratios of 16/7/1/1, respectively. Indomethacin (1 microgram/ml) inhibited this cyclooxygenase-mediated arachidonic acid metabolism. Dexamethasone (1 microgram/ml) also inhibited this metabolic cascade. Its inhibitory effect was not immediate; preincubation of the tissue with dexamethasone potentiated its inhibitory effectiveness. Cycloheximide (0.1 to 10 microgram/ml) also inhibited prostaglandin production. The inhibitory mechanism by cycloheximide of prostaglandin production was discussed in relation to that by dexamethasone.

6-Ketoprostaglandin F1 alpha↗