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Biomedical subjects

A Koda

Publications and source records attributed to A Koda.

At least 145 records · Page 8Linked to original sources
PubMed1985

The susceptibility of experimental glomerulonephritis in six different strains of mice.

An experimental glomerulonephritis was produced in mice by an injection with a sub-nephrotoxic dose of nephrotoxic serum after immunization with rabbit IgG. In order to examine the susceptibility of disease, we tested the onset of nephritis in 6 different strains (ICR,C57BL/6,C3H,DBA/2, nu/nu and DDY) of mice. Strain C57BL/6 mice indicated the highest susceptibility to the disease with a high degree of reproducibility. The excretion of protein in urine, the elevation of serum cholesterol and blood urea nitrogen level and the decrease of serum albumin were observed in nephritic mice. Typical histopathological changes in the kidney were crescent formation in glomeruli, thickening of glomerular basement membrane and cast of urinary tubuli. Cyclophosphamide, at doses of 5 and 10 mg/kg, inhibited the development of nephritis in C57BL/6 mice. These results suggest that the experimental glomerulonephritis model in C57BL/6 mice is useful for immunopharmacological studies of nephritis.

Animals↗
PubMed1985

Immunoglobulin E antibody production against house dust mite, Dermatophagoides farinae, in mice.

Immunoglobulin E (IgE) antibody production against Dermatophagoides farinae extract (mite antigen) was studied in female BALB/c mice. When mice were immunized with mite antigen and aluminium hydroxide gel (alum) intraperitoneally at intervals of 30 d, good primary, secondary and tertiary IgE antibody responses were observed. In the absence of adjuvant, a subcutaneous injection of mite antigen failed to induce the primary IgE antibody response. However, good IgE antibody responses were observed after the secondary immunization given 30 d after the primary immunization. Furthermore, 5 weekly injections of mite antigen alone also induced the IgE antibody production. Intranasal administrations of mite antigen alone also induced the IgE antibody production in mice. Two exposures to mite antigen, intranasally, were sufficient for eliciting low IgE antibody production. The response was significantly potentiated by the administration of islet-activating protein obtained from culture fluids of Bordetella pertussis. These results indicate that the intranasal administration of mite antigen is very effective for eliciting the IgE antibody production.

Adjuvants, Immunologic↗
PubMed1985

[Effect of Saiboku-to, a blended Chinese traditional medicine, on Type I hypersensitivity reactions, particularly on experimentally-caused asthma].

Effect of Saiboku-to, which has been used for the therapy of bronchial asthma, on Type I hypersensitivity reactions was investigated. Forty eight-hr homologous PCA and antigen-induced histamine release in peritoneal cavities of rats passively sensitized with anti-DNP-As . IgE serum tended to be inhibited by the oral administration of Saiboku-to. On the other hand, 7-day homologous PCA in guinea pigs mediated by anti-BPO-BGG . IgE serum was significantly inhibited with 200 and 500 mg/kg of Saiboku-to given orally 2 hr prior to challenge. In experimentally caused asthma in guinea pigs, 200 mg/kg of Saiboku-to dramatically inhibited decreases in the rate and volume of respiration, and 500 mg/kg of the drug inhibited even an increase in the ratio of expiration time to inspiration time. The Schultz-Dale reaction in guinea pig tracheal muscle was significantly inhibited by the pretreatment with 10(-4) g/ml of Saiboku-to. The antigen-induced histamine release from sensitized guinea pig lung tissue was inhibited by 10(-6) to 10(-4) g/ml of Saiboku-to in a dose-dependent fashion, though the release of SRS-A was not affected. Saiboku-to did not show an antagonistic effect on allergic mediator-induced contraction in guinea pig ileum. From these results, it is considered that Saiboku-to shows an inhibitory activity on the Type I hypersensitivity reaction through the suppression of histamine release.

Anaphylaxis↗
PubMed1984

Carcinogenic activities of hydroxymethyl derivatives of 4-(dimethylamino)azobenzene in the liver of rats, mice, and hamsters.

The carcinogenic activity of 3'-hydroxymethyl-N,N-dimethyl-4-aminoazobenzene (3'-CH2OH-DAB) was studied in Sprague-Dawley rats of both sexes, male ddy mice, and male Syrian golden hamsters. The activity of 2'-CH2OH-DAB and 4'-CH2OH-DAB was studied in male Sprague-Dawley rats. Azo dyes were given in the diet at a concentration of 0.064% for 3 months followed by a stock diet for 1 month; animals were sacrificed 4 months after beginning of the experiment. Liver hyperplastic nodules developed in all 8 male rats (100%) and in all 10 female rats (100%) which received 3'-CH2OH-DAB and in 7 out of 12 male rats (58%) which received 2'-CH2OH-DAB. Hepatocellular carcinomas were produced in 1 out of 8 male rats (13%) and in 1 out of 10 female rats (10%) receiving 3'-CH2OH-DAB. No hepatic lesions were observed in rats receiving 4'-CH2OH-DAB and in mice and hamsters receiving 3'-CH2OH-DAB. These results indicate that a carcinogenic effect of 3'-CH2OH-DAB and 2'-CH2OH-DAB could be detected in rats.

Animals↗
PubMed1984

Mouse ear PCA as a model for evaluating antianaphylactic agents.

Passive cutaneous anaphylaxis (PCA) reaction elicited in ears of male ddY mice was studied by means of assessing dye leakage. In the ear, PCA reaction was more sensitive and reproducible than that in the dorsal skin. The reaction was significantly suppressed by ketotifen, one of antianaphylactic agents.

Animals↗
PubMed1984

Effect of vitamin E on IgE antibody formation in mice.

Effect of vitamin E (alpha-tocopheryl acetate and alpha-tocopheryl nicotinate) on IgE antibody formation in mice was investgiated . Female BALB/c mice were immunized with dinitrophenylated ascaris protein (DNP-As) and aluminium hydroxide gel (alum). Supplementation of vitamin E in diets or oral administration of vitamin E mixed with sesame oil resulted in a suppression of IgE antibody formation. On the contrary to IgE antibody formation, IgM or IgG (hemagglutinin; HA) formation was significantly enhanced. These results indicate that vitamin E is capable of suppressing IgE antibody formation and enhancing non-IgE antibody formation.

Administration, Oral↗
PubMed1984

Effect of (+/-)-2-[p-(2-thenoyl)phenyl] propionic acid (suprofen) on experimental allergic reactions.

The effects of (+/-)-2-[p-(2-thenoyl)phenyl] propionic acid (suprofen), a new anti-inflammatory agent, on experimental allergic reaction and antibody formation were examined. The action was compared with those of ketoprofen, ibuprofen, indomethacin, tranilast, chlorpheniramine, prednisolone and/or cyclophosphamide. Suprofen inhibited homologous PCA in rats, immunological histamine release from rat peritoneal mast cells and guinea pig lung tissues, Forssman cutaneous vasculitis (FCV) and the Arthus reaction in guinea pigs. The potency for inhibition of the PCA reaction was similar to that of ketoprofen and more potent than ibuprofen and trailast. As for the release of anaphylactic mediators, suprofen was less potent than tranilast in terms of histamine release, but not the release of the slow reacting substance of anaphylaxis (SRS-A). Suprofen inhibited FCA more potently than other nonsteroidal anti-inflammatory drugs (NSAID). The inhibition of the Arthus reaction by suprofen was similar to those of other NSAID and prednisolone. Suprofen hardly affected delayed hypersensitivity in guinea pigs and antibody (IgM or IgE) formation in mice or rats.

Animals↗
PubMed1984

Effect of N-5' on histamine release from rat peritoneal exudate cells induced by calcium ionophore and ATP.

We studied the effect of N-(3,4-dimethoxycinnamoyl)anthranilic acid (N-5'), an orally applicable anti-allergic drug, on the histamine release induced by calcium ionophores (A23187 and X537A) and ATP from rat peritoneal exudate cells (PEC). X537A (0.1-33.3 micrograms/ml) induced histamine release in a concentration-related manner, and 2.0 micrograms/ml of X537A induced release to the same extent as allergic histamine release. Histamine release induced by 2.0 micrograms/ml of X537A increased with longer incubation time, reaching a peak of about 100% at 120 min. N-5' had no effect on histamine release induced by X537A at the concentrations used (1-1000 microM), but DSCG exhibited significant inhibition at 1-100 microM. A23187 (0.05-0.5 microgram/ml) induced histamine release in a concentration-related manner, and it seemed that 0.033 microgram/ml of A23187 induces the same degree of histamine release as the allergic one. A23187 induced rapid histamine release which attained maximum 1 min after the addition. N-5' exhibited a significant concentration-dependent inhibitory effect on histamine release induced by A23187, and DSCG also exhibited significant inhibition (10 and 1000 microM). N-5' significantly inhibited histamine release induced by 100 microM ATP. These results indicate that N-5' and DSCG effect the histamine release induced by ionophore A23187 and X537A by different manners, and they suggest the possibility that N-5' inhibits some Ca++-dependent processes in histamine release, including the influx of Ca++ into cells, which is a trigger of the A23187 and ATP effects.

Adenosine Triphosphate↗
PubMed1984

The effect of 6-amidino-2-naphtyl-4-guanidinobenzoate dimethane sulfonate (FUT-175) on experimental glomerulonephritis in mice.

Effect of 6-amidino-2-naphtyl-4-guanidinobenzoate dimethane sulfonate (FUT-175) on experimental glomerulonephritis in mice was studied. Employed models are nephrotoxic serum (NTS) nephritis in ddY or A/He mice, rabbit IgG (RGG) accelerated NTS nephritis in ddY mice and spontaneous nephritis in (NZB x NZW) F1 mice. The severity of nephritis was evaluated by measuring proteinuria and serological parameters and examining renal tissue by light microscopy. Therapy with FUT-175 clearly prevented the pathological changes of proteinuria and serological parameters in all four nephritis models. By contrast, treatment hardly affected histopathological changes of the kidney in any of the models. Cyclophosphamide used as a comparative drug showed more clearly remission of the onset and development of NTS nephritis and RGG accelerated NTS nephritis in ddY mice by means of the changes of urinary and selorogical parameters. These evidences suggest that FUT-175 shows beneficial effects on the nephritis in either normal or complement deficient mice.

Animals↗
PubMed1983

Immunopharmacological studies on experimental glomerulonephritis.

Immunopharmacological studies on modified nephrotoxic serum (NTS) nephritis in rats were conducted. The modified NTS nephritis was produced by an intravenous (i.v.) injection of NTS in a subnephrotoxic dose (sub-dose) into the rats which had been previously immunized with rabbit IgG (RGG) and complete Freund's adjuvant (CFA). In previously immunized rats, typical nephritic syndrome was demonstrated with respect to the elevation of urinary protein, serum cholesterol, blood urea nitrogen (BUN) and histopathologic scores of the kidneys. No changes in complement levels were found. By adoptive transfer experiments, it was found that sensitized lymphocytes were essential for causing the nephritis. The potency of the sensitized lymphocytes was reinforced by passing them through a nylon wool or Sephadex G-10 column after treatment with rabbit anti-rat F(ab')2 antibody and complement. The administration of cyclophosphamide, prednisolone, tilorone or cis-1-methyl-4-isohexylcyclohexane carboxylic acid (IG-10) showed a clear remission of nephritis. Cobra venom factor (CoVF) and Cu-chlorophyllin complement inhibitors showed a contradictory efficacy on the nephritis. CoVF which decreased the serum CH50 value did not produce any remission of the nephritis, whereas Cu-chlorophyllin, which slightly decreased CH50 values produced a significant decrease in urinary protein and serum cholesterol. The macrophage-toxic agents carrageenan and dextran sulfate, also did not produce a remission of nephritis. These findings suggest that the participation of T cells is important for the onset of this nephritis and that macrophages and complement do not appear to be involved.

Animals↗
PubMed1983

Immunopharmacological studies on mydocalm and related compounds as an antagonist of slow reacting substance of anaphylaxis (SRS-A).

The antagonistic effect of 2,4'-dimethyl-3-piperidino propiophenone hydrochloride (Mydocalm) and its 15 derivatives against the activity of slow reacting substance of anaphylaxis (SRS-A) were examined in vitro. Mydocalm, 2-methyl-3-piperidino-beta-propionaphthone hydrochloride (As-5) and 2,3',4'-trimethyl-3 piperidinopropiophenone hydrochloride (As-14) were found to be potent antagonists to SRS-A. The above three compounds inhibited homologous passive cutaneous anaphylaxis (PCA) in rats and guinea pigs but not heterologous PCA in guinea pigs. As-5 inhibited the release of histamine from and the degranulation of rat mesenterium mast cells. As-14 also showed the inhibition of the degranulation. Mydocalm, however, showed no inhibition of these reactions. Experimental asthma in guinea pigs which were passively sensitized with guinea pig immunoglobulin E antibody was significantly inhibited by p.o. administration of Mydocalm, As-5 or As-14 respectively.

Animals↗
PubMed1983

Anti-tumor effect of new 5-fluorouracil derivatives and their influences on the immune response.

Authors have previously shown that alpha-mercaptopropionylglycine (alpha-MPG) and sodium dipropylacetate (DPA) facilitate immunity as well as host-mediated anti-tumor activity. In this study, we found that a compound related to alpha-MPG and DPA, (2-n-propyl-n-pentanoyl)glycine (KN-539), inhibited the growth of E.L.4 lymphosarcoma transplanted in C57BL/6 mice and further investigated the anti-tumor effects of 1-(4-carboxy-n-neptyl)-5-FU (KN-826) and 1-(4-carboxymethylaminocarbonyl-n-heptyl)-5-FU (KN-827), in which DPA and KN-539 were combined, respectively, to 5-fluorouracil (5-FU). KN-827 showed stronger anti-tumor activity than KN-826, and it was also effective with oral administration. Although KN-827 demonstrated anti-tumor activity two to three times weaker than N1-(2-tetrahydrofuryl)-5-FU (FT-207), KN-827 did not reduce the blood leukocyte count and the number of spleen cells. Furthermore, KN-827 stimulated the production of the hemolytic plaque forming cell (HPFC) in the spleen of mice immunized with sheep-erythrocytes. In contrast, FT-207 and 5-FU obviously reduced not only HPFC-production but also the number of spleen cells.

Administration, Oral↗
PubMed1983

Pharmacological studies on newly synthesized anti-allergic agents, 2-methyl-3-piperidino-beta-propionaphtone hydrochloride (KZ-111) and 3-isobutyryl-2-isopropylpyrazole-[1, 5-a] pyridine (KC-404).

Effects of 2-methyl-3-piperidino-beta-propionaphtone hydrochloride (KZ-111), 3-isobutyryl-2-isopropylpyrazolo-[1, 5-a]pyridine (KC-404) and FPL-55712 on experimental allergic reactions were investigated. Homologous passive cutaneous anaphylaxis (PCA) in rats was clearly inhibited by oral and intravenous administrations of KC-404 and KZ-111. FPL-55712 inhibited the PCA reaction only by intravenous injections, but not by oral administration. Maximum inhibition of the PCA reaction by KC-404 and KZ-111 was obtained by administration of these agents 2 hr prior to challenge. The immunological release of histamine from sensitized rat peritoneal mast cells was inhibited by KZ-111 at a concentration of 10(-4) g/ml. KC-404 and FPL-55712 did not inhibit the immunological release of histamine. All three compounds had no effect on the release of histamine from rat peritoneal mast cells and on the generation of SRS from rat polymorphonuclear leucocytes by calcium ionophore A23187. KC-404 and KZ-111 produced a downward displacement of the maximum without a parallel shift in LTD4 induced concentration-response curves of guinea pig ileal and tracheal smooth muscle at concentrations between 10(-6) and 10(-5) g/ml. FPL-55712 at a concentration of 10(-6) g/ml produced a parallel shift of LTD4 induced concentration-response curves to the right in both smooth muscle preparations. The 50% inhibitory concentration to the contraction by LTD4 of each of the three compounds is lower than those of other agonists, histamine, PGF2 alpha and BaCl2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Anti-allergic action of glucocorticoids in rats.

The effects of three glucocorticoids (steroids: hydrocortisone, prednisolone and dexamethasone) on IgE antibody-mediated immediate hypersensitivity reactions in rats were studied. Forty-eight hr homologous passive cutaneous anaphylaxis (PCA) was inhibited in a dose response manner by the administration of steroids 2 hr prior to challenge. When steroids were administered at various times before challenge, each steroid showed different patterns of time courses for inhibition of homologous PCA. Maximum inhibition was obtained 2 hr after the administration of each steroid. The IgE antibody-mediated histamine release from peritoneal mast cells in vivo was inhibited by the administration of steroids. Time-courses for the inhibitory effects of steroids on histamine release were slightly different from those in PCA. The increase of capillary permeability caused by histamine, serotonin, trypsin or hyaluronidase in the rat skin was not affected by steroids. The inhibitory action of steroids on PCA was not influenced by non-corticoidal steroids (17 alpha-methyltestosterone, androstenedione and progesterone) or arachidonic acid. These results partially explain the inhibitory action of steroids on IgE antibody-mediated immediate hypersensitivity. The inhibition of histamine release would contribute towards the anti-allergic action of steroids but not the antagonistic effect on the mediators. Also the action of glucocorticoids receptor or the inhibition of arachidonic acid production are not vitally important in connection with the anti-allergic action of steroids.

Animals↗
PubMed1983

Immunopharmacological studies of sodium copper chlorphyllin (SCC).

Effect of sodium copper chlorophyllin (SCC) on experimental allergic reaction was investigated. IgE antibody mediated reactions, homologous passive cutaneous anaphylaxis (PCA) in rats and the release of anaphylactic mediators (histamine and/or slow reacting substance of anaphylaxis (SRS-A] from sensitized guinea pig lung tissues or rat peritoneal mast cells classified as a Type I reaction were clearly inhibited by SCC at a similar potency as N-(3',4'-dimethoxy cinnamoyl) anthranilic acid (N-5'). The increase of vascular permeability in rat skin caused by autacoids or enzymes that participate in the Type I reaction was also inhibited by SCC. Type II or III, complement dependent, reactions including reversed cutaneous anaphylaxis (RCA) in rats and Forssman cutaneous vasculitis (FCV) in guinea pigs were inhibited by SCC. Prednisolone inhibited RCA in rats, but did not inhibit FCV in guinea pigs. Two experimental types of glomerulonephritis, nephrotoxic serum (NTS) nephritis in rats and immune complex nephritis in (NZW X NZB) F1 mice, in which Type II and III reactions might participate in the onset and the development of the disease, were slightly inhibited by SCC in terms of the biochemical changes of blood and urine parameters and histopathological scores. A moderate remission of the onset and development of these two experimental types of nephritis was recognized by the administration of prednisolone. Delayed hypersensitivity reaction as a Type IV reaction caused by sheep red blood cells (SRBC) in sensitized mouse footpad was not affected by SCC. Prednisolone clearly inhibited the SRBC induced footpad reaction in mice. IgM antibody production in mice and IgE antibody production in rats were not influenced by daily injection of SCC.

Animals↗
PubMed1983

Studies on the mechanisms of the inhibitory effect of N-5' on histamine release from rat peritoneal exudate cells.

To investigate the mechanisms for the inhibition of IgE-mediated histamine release from rat peritoneal exudate cells (PEC) by N-5', we studied the relation between the inhibitory effect of N-5' on histamine release and the intracellular levels of adenine nucleotides such as ATP and cAMP. Evident histamine release was induced by the addition of specific antigen to rat PEC sensitized with IgE antiserum in vitro, and the release showed a maximum 30 sec after the antigen challenge. In the same time course as the histamine release, the intracellular levels of ATP and cAMP decreased. N-5' significantly inhibited the histamine release and a decrease in ATP level as a result of the antigen-antibody reaction. A decrease in cAMP level showed a tendency to be suppressed by N-5'. Antigen-induced 14CO2 production for 6-14C-glucose in the sensitized PEC was 3 times that seen in the case without antigen. N-5' dramatically suppressed the acceleration in the production of 14CO2. Differing from the action of papaverine, the inhibitory effect of N-5' on the IgE-mediated histamine release from rat PEC was identical both in the presence or in the absence of glucose. N-5' scarcely affected the ATP level in the non-sensitized PEC in the glucose-free medium. On the other hand, N-5' inhibited the activity of Na+, K+-ATPase, one of the ATP-consuming enzymes, in a dose-dependent fashion. From these results, it is presumed that the suppression of ATP-utilization through the inhibition of Na+, K+-ATPase activity is involved in the inhibition of histamine release by N-5'. The relation between the inhibitory effect of N-5' on histamine release and both nucleotides was also discussed.

Adenosine Triphosphate↗