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Biomedical subjects

H Suda

Publications and source records attributed to H Suda.

At least 271 records · Page 15Linked to original sources
PubMed1985

Effects of glycoprotein synthesis inhibitor on myelination in rat cerebellum.

Effects of a glycoprotein synthesis inhibitor on myelination were investigated in rat cerebellum. The glycoprotein synthesis inhibitor, tunicamycin (TM), was injected intracranially into newborn rats. The activity of 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) in the cerebellum was significantly reduced in 2-week-old animals and was restored to the normal level by age 3 weeks. When TM was injected into newborn rats every 3-4 days for a total of 6 times, CNPase activity was still low at 3 and 4 weeks. Immunohistochemical stainings for CNPase and myelin-associated glycoprotein (MAG) were performed on paraffin sections of multiple-TM-injected cerebellum at 3 weeks. The intensity of the staining with MAG antiserum in the white matter was clearly decreased in TM-treated cerebellum compared with the control. The myelin in the granule cell layer was poorly stained with CNPase antiserum in TM-treated cerebellum. Subcellular fractionation was carried out and the CNPase activity in each fraction was measured. The CNPase activity in the myelin fraction (P2A) from the TM-treated cerebellum was significantly lower than that in the control. In contrast, the activity in the synaptosomal (P2B) and microsomal (P3) fractions from the multiple-TM-injected cerebellum was higher than in those from the controls. Polyacrylamide gel electrophoretic patterns of the P2A fractions were analyzed. The P2A fraction from TM-treated cerebellum contained less Wolfgram protein than the control. These results suggest that glycoprotein synthesis plays certain roles in myelination in the central nervous system.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1985

[Pharmacological studies on N-(2-mercapto-2-methylpropanoyl)-L-cysteine(SA96). IV. Effects of SA96 and its main metabolite, SA679, on denaturation of human gamma-globulin and adjuvant arthritis in rats].

SA96 and its main metabolite, SA679, were investigated for their effects on denaturation of human gamma-globulin and bovine serum albumin (BSA) and on adjuvant arthritis in Lewis rats. The heat denaturation of human gamma-globulin and BSA enhanced by Cu2+ was inhibited by SA96, SA679 and D-penicillamine, and the inhibitory effect of SA96 was the most potent. In adjuvant arthritis rats, SA96 given orally at a dose of 10 mg/kg from the same day as the adjuvant injection inhibited significantly the swelling of adjuvant treated foot and untreated foot, increase of the relative organ weights of the adrenals, liver and kidney, and increase of serum Cu concentration; but at a dose of 100 mg/kg, it did not show any effects on these parameters. On the other hand, SA96 given from three days before the adjuvant injection showed the inhibitory effects at a dose of 100 mg/kg as well as 10 mg/kg. These results suggest that the effect of SA96 on adjuvant arthritis in rats depends on its administration schedule. SA679 also inhibited the adjuvant arthritis at a dose of 100 mg/kg, but its effect was less potent than that of SA96.

Animals↗
PubMed1985

Pharmacological studies of N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96) (3). Effects of SA96 on experimental allergic reactions.

The effects of an antirheumatic agent, N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96), were investigated on allergic reactions in rats and guinea pigs. The effects of SA96 were compared with those of D-penicillamine (D-Pc). SA96 given twice orally at the doses of 10 to 50 mg/kg significantly caused inhibitions of 28%, 29% and 44% against passive cutaneous anaphylaxis (PCA), reversed cutaneous anaphylaxis (RCA) and reversed passive Arthus (RPA) reactions, which are classified as Type I, Type II and Type III allergic reactions, respectively. D-Pc also showed inhibitions of 30%, 23% and 18% on Type I, Type II and Type III reactions, respectively, and inhibitions on Type II and Type III reactions were not significant. On the other hand, SA96 (10 to 50 mg/kg twice) had no influence on the Type IV allergic reaction, delayed hypersensitivity, while D-Pc (20 mg/kg twice) showed an enhancement of 27% on the Type IV reaction. In the in vitro study, SA96 inhibited the hemolytic complement activity at 10(-4) to 10(-2) M and the macrophage migration at 1 X 10(-4) to 5 X 10(-3) M in a dose-dependent manner. These in vitro activities of SA96 were more potent than those of D-Pc. These results showed that SA96 had some different immunopharmacological properties on experimental allergic reactions as compared with those of D-Pc.

Anaphylaxis↗
PubMed1985

Protection against Fasciola gigantica infection in rats administered metacercarial antigens.

Immature worms were recovered from the liver parenchyma of rats which received extracts of metacercariae or adult worms of Fasciola gigantica, after challenge infection. When resistance was assessed by counting the number of immature worms, exposure of the animals to extracts of these two stages of the flukes conferred a significant degree of protection against challenge with F gigantica metacercariae. Rats given the extract of metacercariae were more resistant to infection than rats immunised with the extract of adult worms.

Animals↗
PubMed1984

2',3'-Cyclic nucleotide 3'-phosphodiesterase activity in the cerebrospinal fluid of patients with demyelinating diseases.

We aimed to study the level of CNPase activity in the cerebrospinal fluid of patients with demyelinating diseases and other neurological diseases, particularly multiple sclerosis, with reference to CSF myelin basic protein content. CNPase activity was measured paper chromatographically using radioactive 2',3'-cAMP as a substrate. Myelin basic protein content was measured with a radioimmunoassay. The mean level of CNPase activity was significantly higher for multiple sclerosis than for nonneurological controls. Dividing the disease phases of multiple sclerosis into the three periods, the CNPase activity was found to be significantly elevated in the worsening period and reduced in the improving period and the inactive period. The level of CNPase activity in the cerebrospinal fluid of multiple sclerosis coincided with the clinical activity of the disease. The level of CNPase activity correlated well (r = 0.84) with the level of myelin basic protein content in cerebrospinal fluid. The ratio for CNPase activity and myelin basic protein content in cerebrospinal fluid was almost the same as that in human central nerve myelin. We concluded that CNPase activity in the cerebrospinal fluid from neurological patients is an indicator of destruction of myelin in the central nervous system, and the measurement of CNPase activity in the cerebrospinal fluid of multiple sclerosis could be useful in the clinical management.

2',3'-Cyclic Nucleotide 3'-Phosphodiesterase↗
PubMed1984

Potentiative effect of angiotensin converting enzyme inhibitor on carrageenan edema in rats and the role of tissue kininogen.

Roles of kininogens in the development of potentiation of carrageenan edema in rats by angiotensin converting enzyme (ACE, = kininase II) inhibitor were studied. Carrageenan-induced edema was potentiated by oral administration of YS980, an ACE inhibitor, at a dose of 1 mg/kg 0.5 h before carrageenan injection. Intravenous injection of bromelain, a kininogen (KGN) depletor, at 3 mg/kg produced reduction of plasma KGN (total and high molecular weight KGN), which resulted in suppression of carrageenan edema and suppression of edema potentiation induced by YS980. Even after the plasma KGN level and inflammatory response to carrageenan returned to normal 24 h after the administration of bromelain, the potentiative effect of YS980 on the carrageenan edema remained suppressed. Thus, some factor other than plasma KGN is thought to be involved in the potentiation mechanisms on the carrageenan edema by YS980. Partially purified KGN from rat plasma (0.1 mg/site: liberated 4.4 X 10(-8) g bradykinin eq by trypsin digestion) completely restored the suppressed potentiation to normal by local preinjection to the inflamed site. In addition, such restoration was not observed in the animal in which plasma KGN was reduced 3 h after administration of bromelain. These results suggest that KGN, not only in plasma but also in tissue, play an active role in the development of potentiation of carrageenan edema by ACE inhibitor.

3-Mercaptopropionic Acid↗