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Volume 104 (1994)
- Issue 6 Pages 425-
- Issue 5 Pages 363-
- Issue 4 Pages 275-
- Issue 3 Pages 143-
- Issue 2 Pages 67-
- Issue 1 Pages 1-
Volume 104, Issue 4
Displaying 1-8 of 8 articles from this issue
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Shokei KIM, Kenjiro YAMAMOTO1994 Volume 104 Issue 4 Pages 275-284
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSRecent developments in the techniques of molecular biology and the availability of inhibitors of the renin-angiotensin system have provided new insight into renin-angiotensin research. The control mechanism of renin release and the metabolism of circulating renin have been well characterized on the molecular level. Angiotensin II has been shown to play an important role not only in the regulation of blood pressure but also in cell growth and hypertrophy. ACE inhibitors are effective for the treatments of hypertension and heart failure. Furthermore, recent studies suggest that ACE inhibitors may prevent atherosclerosis and glomerulosclerosis. Angiotensin II receptor antagonists have similar beneficial effects. These effects of ACE inhibitors and angiotensin 11-receptor antagonists may be mediated by growth factors and the extracellular matrix.View full abstractDownload PDF (20477K) -
Chihiro TOHDA, Yasuyuki NOMURA1994 Volume 104 Issue 4 Pages 285-291
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSSynaptic plasticity, a physiological basis of learning and memory, is mainly classified into two categories: 1) relatively short-term changes in electrical activities and 2) more long-lasting morphological changes in synapses. Studies on neuronal differentiation have provided detailed clarification of many of the morphological changes in synapses. Although it has been demonstrated that neuronal differentiation is induced by a variety of stimuli, the mechanism of neuronal differentiation has never been sequentially understood. Since there must be unknown factors relevant to these complicated processes, it is important to find and identify the novel intracellular factors that are able to induce the differentiation of neurons. Differential screening is useful cloning method to identify molecules without any information about their structures. Genes expressed in a distinct pattern among two or more groups, eg. different drug-treated cells, tissues and so on, can be isolated. To identify novel neuronal differentiation factors, we differentially screened approximately 500, 000 primary clones from the cDNA library of NG108-15 cells treated with TPA and diBu-cAMP for 72 hr. Using two single strand cDNA probes, which were reverse-transcribed from poly(A)+RNA, TA-20 was isolated from cells treated with TPA and diBu-cAMP (probe TA) or from cells treated with diBu-cAMP alone (probe A) for 72 hr. Clones that hybridized preferentially to the probe TA were further investigated by Southern and Northern blots. Thus the identified clone TA20 is a novel gene and plays functional roles as a neuronal differentiation factor.View full abstractDownload PDF (12380K) -
Nobuo KOSAKA, Hiroshi TANAKA, Akio ISHII, Katsuichi SHUTO1994 Volume 104 Issue 4 Pages 293-302
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effects of 5-[2-(diethylamino)ethyl]amino-5, 11-dihydro[1]benzoxepino[3, 4-b]pyridine trihydrochloride (KW-5805) on the changes of gastric mucus induced by stress and aspirin were studied in rats. Water immersion-restraint stress time-dependently decreased the gastric adherent mucus content and induced gastric ulcers. Aspirin, administered orally at 200 mg/kg, reduced the gastric adherent mucus level and produced gastric erosions. The diminution of gastric mucus reached a maximum at 3 hr, and a gradual return to the non-treatment value was observed subsequently. Pretreatment with KW-5805, given orally at 3, 10 or 30 mg/kg, dose-dependently prevented stress- and aspirin-induced mucus depletion and gastric ulceration. Gastric mucus glycoprotein levels, indicated by the contents of hexose and hexosamine, were also decreased by aspirin. KW-5805 pretreatment (30 mg/kg, p.o.) significantly inhibited the diminution of mucus glycoproteins. KW-5805 also increased the gastric adherent mucus content and the amount of glycoproteins in normal rats. These results suggested that the stimulating effects of KW-5805 on the secretion and storage of gastric mucus may account for some of its antiulcer properties.View full abstractDownload PDF (19193K) -
Koichi NAKAMARU, Toshiji SUGAI, Takayuki HONGYO, Masako SATO, Sugure T ...1994 Volume 104 Issue 4 Pages 303-311
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSMesalazine microgranules are an ethylcellulose-coated formulation from which mesalazine is released throughout the intestinal tract and are expected to be effective for idiopathic inflammatory bowel disease, ulcerative colitis and Crohn's disease. Mesalazine microgranules were administered orally to investigate the distribution of mesalazine throughout the intestinal tract in rats. Mesalazine microgranules distributed sufficient amounts of mesalazine and its metabolite, N-acetyl-mesalazine, to the intestinal tissues, while pure mesalazine delivered lower amounts of both. In acetic acid-induced colitis in rats, mesalazine microgranules administered orally reduced the damage score significantly (P<0.05) at a dose of 50 mg/kg as assessed by macroscopic observation and at 100 mg/kg as assessed by histological evaluation. The number of ulcers in carrageenan-induced colitis in guinea pigs was inhibited at doses of 50, 100, 200 mg/kg, p.o. The colonic wet weight of rats in 2, 4, 6-trinitrobenzenesulfonic acid (TNB)-induced colitis was reduced significantly (P<0.05) at a dose of 50 mg/kg, p.o. Mesalazine microgranules showed the ability to distribute mesalazine efficiently throughout the intestinal tract and showed effectiveness against acetic acid-, carrageenan- and TNB-induced colitis. These studies strongly suggest that mesalazine microgranules are effective for idiopathic inflammatory bowel disease.View full abstractDownload PDF (18830K) -
Kenjiro MOMO, Kohei HOSHINA, Yuji ISHIBASHI, Takao SAITO1994 Volume 104 Issue 4 Pages 313-323
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe have developed a unique rat AGML model produced by ischemia/reperfusion plus 0.2% ammonia (I/R·NH3), either treatment which would not induce mucosal injury when used alone. The effects of troxipide and other gastric mucosal defensive drugs were investigated with this I/R·NH3-induced AGML model and other AGML models in rats. The following results were obtained: 1) Like allopurinol, troxipide at 50-200 mg/kg, p.o. dose-dependently prevented I/R·NH3-induced development of AGML and also the ischemia/reperfusion-induced increase of gastric mucosal thiobarbituric acid (TBA)-reactive substances; 2) Troxipide at 10-6-10-4 M, like allopurinol, inhibited concentration-dependently in vitro xanthine oxidase activity in gastric mucosal homogenates; 3) Troxipide at 50-200 mg/kg, p.o. inhibited AGMLs induced by bleeding plus 0.2% ammonia and by 1.0% ammonia alone; and 4) Troxipide and sofalcone were similar in preventing all AGMLs tested and also the increase of mucosal TBA-reactive substances, but somewhat differed from teprenone, cetraxate hydrochloride, azulene plus L-glutamine and sucralfate. These findings suggest that troxipide may inhibit I/R·NH3-induced AGML development by preventing generation of oxygen free radicals and by protecting against mucosal fragility due to reduced energy metabolism from poor blood flow and also against ammonia-induced disruption of the gastric mucosal barrier. Therefore, troxipide may be highly effective for various AGMLs with multifactor involvement.View full abstractDownload PDF (24015K) -
Makoto MASUDA, Aoi UCHIDA, Hitoshi MATSUKURA, Toshiro KAMISHIRO1994 Volume 104 Issue 4 Pages 325-335
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSInhibitory action of leminoprazole ((±)-2-[[2-(isobutylmethylamino)benzyl]sulfinyl]-1H-benzimidazole, NC-1300-O-3, LEM) against the H+, K+-ATPase activity in rabbit gastric vesicles was investigated. LEM inhibited the H+, K+-ATPase activity in leaky vesicles in a concentration and time-dependent manner. When preincubated with gastric vesicles (20 μg protein/ml) for 30 min at 37®C in medium (pH 6.1 or 7.4), the IC50 values were 5.3 μM and 19 μM, respectively. The inhibitory action of LEM was not competitive with respect to K+ and was not reversed by dilution, suggesting that the inhibitory action is irreversible. Inhibition of the enzyme activity by LEM was not found when β-mercaptoethanol (0.1 mM) was premixed with enzyme before addition of LEM, and it was partially recovered by addition of β-mercaptoethanol or dithiothreitol (50 mM) after LEM treatment. These results suggest that LEM reacts with essential SH groups of H+, K+-ATPase and inactivates the enzyme by forming a covalent disulfide bond. The inhibitory activity of LEM was more potent at pH 6.1 than at pH 7.4, and the rate of the reaction of LEM with GSH was enhanced by lowering the pH of the medium. The inhibition of proton transport by LEM (30 μM) was found after the intact vesicles were fully acidified. LEM also strongly inhibited the valinomycin-stimulated H+, K+-ATPase activity. Therefore, it is considered that LEM inhibits H+, K+-ATPase activity by an unknown activated reaction under the acidic condition. Alternatively, the possibility was also suggested that an acidic condition is not always necessary for the inhibition of H+, K+-ATPase activity by LEM, since LEM, at higher concentration, inhibited the initial rate of acidification and inhibited nigericin-stimulated H+, K+-ATPase activity in intact vesicles.View full abstractDownload PDF (21150K) -
Kaname MIYAMOTO, Jun-ichi NAGAKAWA, Naoko NAGAOKA, Ieharu HISHINUMA, J ...1994 Volume 104 Issue 4 Pages 337-345
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe studied the effect of E3123 on pancreatic injury induced in the isolated, perfused pancreas or in a pancreatic slice. Exposure of the isolated, perfused rat pancreas to trypsin-taurocholate or phospholipase A2 caused the leakage of pancreatic enzyme (lipase) into the perfusate. In trypsin-taurocholate-induced pancreatic injury, E3123 and nafamostat mesilate suppressed the leakage of lipase at concentrations of 0.1-1μM and 1-10μM, respectively. In phospholipase A2 induced pancreatic injury, E3123 at 10 μM significantly suppressed the enzyme leakage, and nafamostat mesilate had a weak suppressive effect. Exposure of a rat pancreatic slice to phospholipase A2 also caused the leakage of pancreatic enzyme, while the inhibition of enzyme leakage by E3123 was similar to that observed in the isolated, perfused pancreas; nafamostat mesilate was not effective. This finding suggests the possible involvement of a unique mechanism of action in the protection against pancreatic injury by E3123. Therefore, we studied the effect of E3123 on hemolysis by osmotic shock using rat red blood cells. E3123 demonstrated a potent protective effect against the hemolysis, suggesting that a membrane-stabilizing action may contribute to the protection E3123 affords against pancreatic injury.View full abstractDownload PDF (15719K) -
Takumi IMAI, Hirofumi KAI, Yoichiro ISOHAMA, Kazuo TAKAHAMA, Takeshi M ...1994 Volume 104 Issue 4 Pages 347-355
Published: 1994
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effects of a novel antiallergic drug, quinotolast (FK021, sodium 5-(4-oxo-1-phenoxy-4H-quinolizine-3-carboxamido)tetrazolate monohydrate), on airway clearance was studied in comparison with those of tranilast (an orally-active antiallergic drug). FK021 (10 mg/kg, p.o.) did not influence the rabbit airway secretion, whereas tranilast (100 mg/kg, p.o.) caused a slight suppression. Neither FK021 (10-10-10-5 g/ml) nor tranilast (10-6, 10-4 g/ml) had any effect on pulmonary surfactant secretion in rat type II pneumocytes. FK021 (10 mg/kg, p.o.) caused a significant increase in the mucociliary transport rate in quails, whereas tranilast (320 mg/kg, p.o.) had no effect. Antitussive effects were examined in normal guinea pigs and guinea pigs made bronchitic by an exposure to SO2. FK021 (10 mg/kg, p.o.) and tranilast (320 mg/kg, p.o.) significantly depressed the cough reflex induced by citric acid in normal animals. FK021 (32 mg/kg, p.o.), but not tranilast (320 mg/kg, p.o.), showed antitussive effects on citric acid-induced cough in bronchitic animals. These results suggest that FK021 may have favorable effects on expectoration and cough reflex observed in the patients with chronic obstructive pulmonary diseases such as asthma.View full abstractDownload PDF (16675K)
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