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Biomedical subjects

A Koda

Publications and source records attributed to A Koda.

At least 163 records · Page 9Linked to original sources

Isolation and chemical properties of a haptenic substance from buckwheat dialysate.

A haptenic substance was isolated from the dialysate of the aqueous extract of buckwheat. This substance, BWD II 22-3, which was composed of Asp(1), Thr(1), Ser(1), Gly(1), Gly(4), Ala(1), Val(1), Leu(1), Orn(2), Lys(1), Arg(1), Cys(1) and glucose was demonstrated to be homogeneous by gel filtration and paper electrophoretic analyses. The molecular weight was estimated to be 1600 by gel filtration on Sephadex G-50. The haptenic substance apparently has-SH group determinant caused about 50% inhibition at a concentration of 100 micrograms/disc in the RAST procedure using human serum sensitive to buckwheat. An active component, BWD II 22-3, might prove effective in the hyposensitization therapy of buckwheat-sensitive patients.

Desensitization, Immunologic↗

Experimental glomerulonephritis in mice as a model for immunopharmacological studies.

The experimental glomerulonephritis was caused by the intravenous injection of a subnephrotoxic dose of nephrotoxic serum in the mice which had been previously immunized with rabbit IgG and complete Freund's adjuvant. The elevation of urinary protein excretion, serum blood urea nitrogen level and cholesterol level and the decrease of serum albumin level were demonstrated in nephritic mice. Hypercellularity in the glomerulus and hyalinosis in tubular system were observed in histopathological studies. The clinical signs in this experimental model were similar to human glomerulonephritis. In a transfer experiment, sensitized lymphocytes against rabbit IgG were necessary for the onset of disease. Clear remission of glomerulonephritis was indicated by the administration of cyclophosphamide or 6-mercaptopurine. Glucocorticoids showed moderate suppression of the development of this nephritis. These evidences suggest that this experimental model is useful for the immunopharmacological research of glomerulonephritis.

Animals↗

Immunopharmacological studies of the aqueous extract of Cinnamomum cassia (CCAq). I. Anti-allergic action.

Effect of the aqueous extract of Cinnamomum Cassia (CCAq) on experimental allergic reaction was investigated. IgE mediated reactions, homologous passive cutaneous anaphylaxis (PCA), degranulation of mast cells, and the release of histamine from sensitized lung tissues classified as the type I reaction by Coombs and Gell were not affected by CCAq. Complement dependent reactions including reversed cutaneous anaphylaxis (RCA), Forssman cutaneous vasculitis (FCV), and nephrotoxic serum (NTS) nephritis classified as type II and the Arthus reaction classified as type III were clearly inhibited by CCAq. However, CCAq did not affect the nephritis caused by the F(ab')2 portion of the nephrotoxic IgG antibody. CCAq in a high concentration inhibited the immunological hemolysis, chemotactic migration of neutrophils in response to complement activated serum, and the generation of chemotactic factors. The type IV reaction, contact dermatitis, was not affected by CCAq. The production of hemolytic plaque forming cells was slightly inhibited by CCAq. These results suggest that CCAq has an anticomplement action and inhibits the complement dependent allergic reaction.

Animals↗

Immunopharmacological studies of the aqueous extract of Cinnamomum cassia (CCAq). II. Effect of CCAq on experimental glomerulonephritis.

Effect of the aqueous extract of Cinnamomum Cassia (CCAq) on experimental glomerulonephritis was studied and compared with that of cobra venom factor (CoVF). In rat nephrotoxic serum (NTS) nephritis, CCAq clearly inhibited the excretion of protein into the urine and the increase of peripheral leucocyte counts. The histological score in CCAq administered animals was significantly lower than that in control animals. However, CCAq did not inhibit or lower the serum complement level. Contrary to CCAq, hypocomplementation was observed by the administration of CoVF, and the excretion of protein into urine was inhibited in a high dose group. In immune complex (IC) and autologous IC nephritis in rats, CCAq clearly inhibited the excretion of protein into urine and the elevation of blood urea nitrogen (BUN). The administration of CoVF caused hypocomplementation, but little inhibition of the excretion of urinary protein was observed in both types of immune complex nephritis. The histological score was slightly inhibited by a low dose of CCAq and a high dose of CoVF. In the experiment employing NZB/NZW F1 mice, the proteinurea, the elevation of BUN level, and the production of antibodies were clearly inhibited by the administration of CCAq. Similar inhibition was observed by CoVF at a high dose. However, the histological changes of the kidney in NZB/NZW F1 mice were not prevented by the administration of CCAq or CoVF.

Animals↗

[Anti-allergic actions of traditional oriental medicine--actions against types I and IV hypersensitivity reactions].

A study was carried out to examine the effects of 23 kinds of crude drugs and 3 kinds of blended Chinese traditional medicines on Type I and Type IV allergic reactions. Forty eight-hr homologous PCA in rats as a typical model of the Type I reaction using anti-dinitrophenylated ascaris . IgE serum was significantly inhibited by the oral administration of the following drugs: Aqueous extracts: Aurantii F.i., Bupleuri R., Schizandrae F., Scutellariae R., Zizyphi F., and Shohsaiko-to and Methanolic extracts: Asiasari R., Aurantii F.i., Bupleuri R., Ginseng R., Glycyrrhizae R., Magnoliae C., Schizandrae F. and Trichosanthis S., Contact dermatitis in mice as a model of the Type IV reaction caused by picryl chloride was significantly inhibited by the oral application of aqueous extracts of Ginseng R. and Magnoliae C. as well as the powder of Hoelen. The aqueous extract of Saiboku-to also showed an inhibition of the contact dermatitis, and it significantly potentiated the inhibition of contact dermatitis by prednisolone.

Animals↗

[Effect of neurotropin (NSP) on allergic reactions (author's transl)].

A study was carried out to examine the effect on neurotropin (NSP) on the 4 types of allergic reactions classified by Coombs and Gell. 1) Type 1: NSP inhibited 48-hr homologous passive cutaneous anaphylaxis (PCA) as well as antigen-induced degranulation of rat mesenterium mast cells. The drug also inhibited both experimental asthma and histamine release from lung tissue in guinea pigs, as mediated by IgE antibody. 2) Type 2: NSP slightly suppressed the increase in urinary protein levels caused by nephrotoxic nephritis in rats and showed a tendency to inhibit Forssman shock in guinea pigs. NSP had an anticomplement activity in vitro but did not inhibit the reversed cutaneous anaphylaxis in rats. 3) Type 3: NSP suppressed an increase in the urinary protein level of rats with glomerulonephritis, as induced by immune complex. 4) Type 4: NSP slightly inhibited the increase in the urinary protein level in glomerulonephritic rats pretreated with IgG. However, the drug did not affect picryl chloride-induced contact dermatitis in mice. We conclude that NSP inhibits allergic reactions used in the present study except for reversed cutaneous anaphylaxis and contact dermatitis, and the most potent activity is seen in the case of Type 1 reaction.

Animals↗

Tumorigenicity of 3'-hydroxymethyl, 3'-formyl, and 3'-carboxy derivatives of 4-(dimethylamino)azobenzene in rat liver.

Male Sprague-Dawley rats were fed a cube diet containing 2.51 mmol/kg of 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB), 3'-CH2OH-DAB, 3'-CHO-DAB, or 3'-COOH-DAB (at a level equivalent to 0.06% 3'-Me-DAB in the diet) for a period of 1 to 3 months. Almost all the livers of rats given 3'-CH2OH-DAB for a period of 2 to 3 months or 3'-Me-DAB for 3 months showed marked cirrhosis macroscopically. The common histological findings were cholangiofibrosis with or without markedly atypical bile ducts. Moreover, one hepatocellular carcinoma was found in the liver of a rat given 3'-Me-DAB and one in the liver of a rat given 3'-CH2OH-DAB for 3 months. On the other hand, 3'CHO-DAB and 3'-COOH-DAB did not induce these changes (including neoplastic nodules) at all. Consequently, 3'-CH2OH-DAB, like 3'-Me-DAB, was found to be a hepatocarcinogen.

Animals↗

Role of hyaluronidase in immediate hypersensitivity reaction.

Hyaluronidase (Hydase) activity in 48-hr homologous passive cutaneous anaphylaxis (PCA) increased about one and one-half times the control for 5 min after challenge with antigen, then gradually decreased and disappeared after 30 min. Change in Hydase activity correlated well with the increase in capillary permeability by PCA. DSCG and BPS given intravenously 10 min prior to challenge produced increases in capillary permeability and Hydase activity caused by PCA was inhibited. Chlorpheniramine inhibited the increase of the capillary permeability, but not the acceleration of Hydase. Prednisolone neither affected the capillary permeability nor the Hydase activity. Similar results were also obtained in in vitro studies. An increase in the capillary permeability caused by PCA, histamine, or 5-HT was additionally augmented by Hydase. Thus, Hydase appears to be involved in the increase in the capillary permeability caused by an immediate hypersensitivity reaction.

Animals↗

Carcinogenicity of 3'-hydroxymethyl-N,N-dimethyl-4-aminoazobenzene in rat liver.

Male Sprague-Dawley rats were fed a cube diet containing 2.51 mmol/kg 3'-hydroxymethyl-N,N-dimethyl-4-aminoazobenzene (3'-CH2OH-DAB) for a period of 1 or 3 months. (This is the molar equivalent of 0.06% 3'-Me-DAB in the diet). The oral administration of 3'-CH2OH-DAB for 3 months resulted in a high incidence of liver tumors at 6 months and the 1 month feeding also caused the development of liver tumors. Histologically, the tumors were cholangiocellular carcinomas and hepatocellular carcinomas. The development of tumors in other sites was not seen. Consequently, 3'-CH2OH-DAB, a recently identified metabolite of 3'-Me-DAB, is a potent hepatocarcinogen.

Animals↗

Immunopharmacological approach to Forssman shock.

Forssman shock (FS) following the intravenous injection of antisheep erythrocyte antibody into guinea pigs resulted in fatal systemic shock with marked decrease in CH50 values of complement, leucocyte, and platelet counts, and a prolongation of blood coagulation time. In addition, there was an increase in lactate dehydrogenase activity, and decreases in both esterase activity and fibrinogen levels were noted. F(ab')2 of antisheep erythrocyte IgG antibody was not capable of eliciting FS. Cobra venom factor showed a fairly potent inhibition of FS. Leukopenia induced by cytosine arabinoside given intraperitoneally for 5 days had no effect on FS. Colchicine, which decreased the leucocyte count, did not inhibit fatal systemic shock. Administration of heparin or trasyrol did not prevent FS. The present findings demonstrate that FS is inhibited by anticomplementary agents but not by drugs which affect leucocyte and platelet counts, the coagulation system or serum proteases.

Anaphylaxis↗

Inhibition of homologous passive cutaneous anaphylaxis (PCA) by disodium cromoglycate-related compounds.

A study was conducted to examine the effect on homologous PCA in rats of 14 different, newly synthesized compounds, given orally, in relation to the chemical structure of DSCG, when given orally on homologous PCA in rats. The structure-activity relationship of these compounds was also discussed. Among the 7 compounds of the glycerol bischromenonyl ether derivatives, 1,3-bis (2-phenyl-4-chromenon-5-yl) oxypropane-2-ol (compound 1) showed the most potent inhibitory activity on PCA. The other compounds showed a moderate or no effect. Two compounds of glycerol bisphenyl ether derivatives had little effect. On the other hand, 1,3-bis (2-carboxy-3-hydroxyphenyl)oxypropane (compound 11) out of alkandiol bisphenyl ether derivatives significantly inhibited PCA, and the other 4 compounds showed a tendency toward inhibition of the reaction. The late inhibition, seen in the biphasic inhibitory pattern induced by compound 11, may be caused by a certain active substance transformed in the body.

Animals↗