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  • 1
    ISSN: 1573-2568
    Keywords: cultured rabbit gastric cells ; cytoprotection ; tauroursodeoxycholate ; ursodeoxycholate ; chenodeoxycholate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ursodeoxycholate (UDC) and tauroursodeoxycholate (TUDC) have been reported to be protective against liver injury induced by other bile salts. UDC also has been shown to be effective against refluxed bile-induced gastritis after gastric surgery. However the mechanism of the therapeutic effect of UDC on gastric mucosa has not been known. In the present study, cytoprotective actions of UDC and TUDC against chenodeoxycholate (CDC)-induced gastric injury were investigated using rabbit gastric cell cultures without systemic factors. Rabbit gastric mucosal cells were cultured after the isolation of rabbit gastric cells with collagenase and ethylenediaminetetraacetic acid. Cytotoxicity was quantified by measuring51Cr release from prelabeled cells and MTT assay. Prostaglandin (PG) E2 was assayed by radioimmunoassay. Concentrations of CDC〉0.5mM or UDC〉5mM caused cellular damage and increased51Cr release in a dose-dependent and time-dependent fashion, while TUDC up to 10 mM did not. TUDC, but not UDC, showed a significant decrease of CDC (1.5 mM)-induced51Cr release dose dependently. The protective effect of TUDC against CDC-induced damage was confirmed by MTT assay. On phase-contrast microscopy, disruption of monolayers induced by CDC (1.5 mM) was clearly protected by TUDC (10 mM). Free radical scavengers (500 units/ml of superoxide dismutase, 300 units/ml of catalase, and 100 mM of dimethyl sulfoxide) or a calcium blocker (10−7–10−5 M verapamil) did not show significant protection against CDC-induced damage. Deprivation of Ca2+ in the media did not affect CDC-induced damage. Thus free radicals of Ca2+ might not be involved in the cell toxicity of CDC. Although TUDC (10 mM) significantly increased PGE2 production by cultured cells, indomethacin (10−4 M) did not reduce protective effects of TUDC, as assessed by51Cr release and MTT assay. In conclusion TUDC is cytoprotective against CDC-induced damage to cultured rabbit gastric cells. Neither free radicals, Ca2+, nor endogenous PGs may play leading roles in the mechanism of this action.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of materials science 29 (1994), S. 4081-4085 
    ISSN: 1573-4803
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Notes: Abstract In situ growth of AI2O3 whiskers into the matrix of Y-TZP (yttria-doped tetragonal zirconia polycrystals) was examined in order to prepare Y-TZP/AI2O3 whisker preform for the composites. Various shapes of AI2O3 particles were grown by the reaction of AI2O3 and AIF3 powders with moist nitrogen or oxygen gases at high temperature. They showed a trend to change the particle shapes from massive → rhombohedron → whisker → platelet as the processing temperature was increased. These particles, however, grew only on the surface and not inside the pellets It was found necessary to introduce the carrier gas inside the pellets for particle growth to occur internally. AI2O3 whiskers can be synthesized inside the pellets by mixing with an organic space-forming agent having a relatively large particle size.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: cultured rabbit gastric cells ; prostaglandin E2 release ; protein kinase C ; Ca2+ ; cAMP
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostaglandin (PG) has been reported to be one of the important protective factors in the gastric mucosa. However the mechanism of the regulation of endogenous PG production has not been well studied. We investigated the possible roles of Ca2+, cAMP, and protein kinase C (PKC) in the regulation of PGE2 release from cultured rabbit gastric mucosal cells. PGE2 was measured by radioimmunoassay. A23187 (Ca2+ ionophore) at 2×10−6 M significantly increased PGE2 release. Deprivation of Ca2+ from the medium blocked the A23187-induced increase of PGE2. TMB-8 (a putative inhibitor of Ca2+ release from intracellular stores) did not have any significant effects on the increase of PGE2-induced by A23187. Thus, A23187 increased PGE2 through the influx of extracellular Ca2+. W7 or compound 48/80 (calmodulin inhibitors) did not alter the response of PGE2 caused by A23187. Exogenous administration of cAMP, forskolin (an activator of adenylate cyclase), or 2-chloroadenosine (a possible activator of adenylate cyclase through adenosine A2 receptor) had neither significant effects on PGE2 release nor an effect on A23187-induced increase of PGE2 release. 12-O-tetradecanoylphorbol 13-acetate (TPA, an activator of PKC) significantly stimulated PGE2 release in a dose-dependent fashion, whereas another phorbol ester with no biological activity did not. A23187 at 0.8×10−6 M, but not cAMP, potentiated the TPA-induced increase of PGE2. Mepacrine (a phospholipase A2 inhibitor) reduced the A23187-and TPA-induced increase of PGE2. These results suggest that Ca2+ and protein kinase C may play important roles in the regulation of PGE2 release by cultured rabbit gastric cells.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of materials science 10 (1991), S. 588-590 
    ISSN: 1573-4811
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Type of Medium: Electronic Resource
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