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  • Ovariectomized rat  (1)
  • Steroid  (1)
  • binding to gastric mucosa  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Effect of prostaglandin D2 on the femoral bone mineral density in ovariectomized rats (1993)
    Springer
    Calcified tissue international 52 (1993), S. 442-446 
    Details
    ISSN: 1432-0827
    Keywords: Ovariectomized rat ; In vivo ; Bone mineral density ; Dual energy X-ray absorptiometry ; Prostaglandin D2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Summary We studied the effects of prostaglandin D2 (PGD2) on the femoral bone mineral density (BMD) and other related parameters in ovariectomized (OVx) and shamoperated rats. BMD was measuredin vivo by dual energy X-ray absorptiometry (DXA) for the period of 36 days or 112 days after operation. When 9- or 10-week-old rats were used at the time of operation, the femoral BMD increased during these periods. Ovariectomy resulted in a marked suppression of this steady increase in BMD at both proximal and distal ends of the femur. Subcutaneous administration of a slow-release preparation of PGD2 on days 1 and 21 not only prevented the ovariectomy-induced suppression of BMD, but also augmented the steady increase in BMD of the shamoperated rats. When medication was started on day 70, the depressed rate of increase in BMD was restored to the control level. Serum calcitonin (CT) and parathyroid hormone (PTH) levels were not affected by either ovariectomy or by PGD2 administration. Body weight and bone length were increased, but uterine weight was decreased by ovariectomy. PGD2 administration showed no effects on these parameters. There was a significant increase in the fasting level of urinary hydroxyproline excretion after ovariectomy, and PGD2 administration had no significant effect on this parameter either. These results indicate that the prevention of osteopenia in OVx rats and the increase in BMD in shamoperated and post-OVx rats by PGD2 administration are due to its stimulatory effect on bone formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571334
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Z-350, a new chimera compound possessing α1-adrenoceptor antagonistic and steroid 5α-reductase inhibitory actions (1999)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 359 (1999), S. 433-438 
    Details
    ISSN: 1432-1912
    Keywords: Key words Z-350 ; α1-Adrenoceptors ; Steroid ; 5α-reductase ; Lower urinary tract ; Benign prostatic ; hyperplasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of Z-350, (S)-4-[3-(4-{1-(4-methylphenyl)-3-[4-(2-methoxyphenyl)piperazine-1-yl]propoxy} benzoyl)indole-1-yl]butyric acid hydrochloride, a newly synthesized compound possessing α1-adrenoceptor antagonistic and steroid 5α-reductase inhibitory actions, were studied in vitro. In functional experiments, Z-350 shifted the concentration/response curve for the phenylephrine-induced contraction of rabbit prostate, urethra and aorta to the right with pA2 values of 8.04, 7.57 and 7.13, respectively. The binding affinity of Z-350 for α1-adrenoceptors in rabbit prostate, urethra and aorta were estimated by the displacement of [3H]prazosin. The pK i values for this action of Z-350 were 7.53, 7.95 and 7.62 for the prostate, urethra and aorta, respectively. α1-Adrenoceptor subtype selectivities were studied in the submaxillary gland (α1A) and liver (α1B) of rat. Z-350 inhibited the specific binding of [3H]prazosin to α1A and α1B-adrenoceptors with pK i values of 7.82 and 7.29, respectively. Z-350 inhibited rat prostatic steroid 5α-reductase non-competitively with a pIC50 of 8.42. These results indicate that Z-350 is a α1-adrenoceptor antagonist and is a steroid 5α-reductase inhibitor. It is expected that Z-350 will be a candidate drug for the treatment of benign prostatic hyperplasia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005372
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Relationship between gastroprotective effect of locally acting antiulcer agent ecabet sodium and its binding to gastric mucosa in rats (1995)
    Springer
    Digestive diseases and sciences 40 (1995), S. 661-667 
    Details
    ISSN: 1573-2568
    Keywords: ecabet sodium ; sucralfate ; ethanol-induced gastric lesions ; binding to gastric mucosa ; rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was designed to examine the relationship between the gastroprotective efficacy of the locally acting antiulcer drug ecabet sodium (ecabet) against ethanol-induced gastric lesions and the amount of the drug bound to the mucosa in comparison with sucralfate in rats. Oral administration of ecabet (25–100 mg/kg) and sucralfate (25–400 mg/kg) dose dependently prevented the formation of ethanol-induced gastric lesions, and dose dependently increased the amount of each drug bound to the gastric mucosa. Pretreatment with the antisecretory agent cimetidine (200 mg/kg, per os) significantly reduced the gastroprotective effect of sucralfate in proportion to a decrease in its binding to the mucosa. The same pretreatment tended to reduce both gastroprotection by ecabet and its binding to the mucosa. In anin vitro study using an everted stomach sac, the binding of sucralfate to the mucosa was more markedly decreased than that of ecabet on increasing the pH. These findings indicate that ecabet and sucralfate protect the gastric mucosa against ethanol in proportion to the amount of each drug bound to the gastric mucosa and that the binding of these drugs to the mucosa is under the influence of intraluminal pH. However, the gastroprotective effect of ecabet seems to be less dependent on intraluminal acidity than that of sucralfate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02064387
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    Paper (German National Licenses)
    Fulltext
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