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  • 1
    Electronic Resource
    Electronic Resource
    The molecular mechanism of inhibition of interleukin-1β-induced cyclooxygenase-2 expression in human synovial cells by Tripterygium wilfordii Hook F extract (1999)
    Springer
    Inflammation research 48 (1999), S. 575-581 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Tripterygium wilfordii Hook F — Cyclooxygenase-2 — Glucocorticoid receptor — Nuclear factor-κB — Synovial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: Several extracts of Tripterygium wilfordii Hook F (TWHF) have been reported to be effective in patients with rheumatoid arthritis. We investigated the effect of multi-glycosides of TWHF (GTW), a TWHF extract, on interleukin (IL)-1β-stimulated human rheumatoid synovial cells. ¶Materials and Methods: IL-1β-stimulated synovial cells were used to detect the effects of GTW on cyclooxygenase (COX)-1 and COX-2 activities, expression of COX protein and mRNA, and nuclear transcription factors in experiments using respective reporter plasmids. ¶Results: GTW inhibited prostaglandin E2 production by IL-1β-stimulated synovial cells in a concentration-dependent manner, and also inhibited COX-2 protein and mRNA expression in a similar fashion to dexamethasone. However, GTW did not act as a glucocorticoid agonist. GTW repressed IL-1β-induced nuclear factor-κB activity, but did not have a significant influence on activating protein-1 activity. ¶Conclusion: The anti-rheumatic effect of GTW or TWHF may be partly mediated through the inhibition of prostaglandin E2 production in human synovial cells due to suppression of COX-2 mRNA, possibly via inhibition of nuclear factor-κB activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050506
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Glucagon Induces Suppression of ATP-sensitive K+ Channel Activity Through a Ca2+/Calmodulin-dependent Pathway in Mouse Pancreatic β-Cells (1998)
    Springer
    The journal of membrane biology 166 (1998), S. 237-244 
    Details
    ISSN: 1432-1424
    Keywords: Key words: cAMP — Calmodulin antagonist — Caged Ca2+— Islet of Langerhans — Glycogenolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract. Glucagon is known to increase intracellular cAMP levels and enhance glucose-induced electrical activity and insulin secretion in pancreatic β-cell perfused with Krebs-Ringer bicarbonate solution. The present experiments were aimed at evaluation of the hypothesis that changes in β-cells ATP-sensitive K+ (K(ATP)) channel activity are involved in the glucagon-induced enhancement of electrical activity. Channel activity was recorded using the cell-attached configuration of the patch-clamp technique. Addition of glucagon (2.9 × 10−7 m) in the presence of 11.1 mm glucose caused closure of K(ATP) channels followed by an increase in the frequency of biphasic current transients (action currents) due to action potential generation in the cell. Three calmodulin-antagonists (W-7, chlorpromazine, and trifluoperazine) restored with similar efficacy K(ATP) channel activity in cells being exposed to glucagon. At 2.8 mm glucose, glucagon did not affect K(ATP) channel activity until Ca2+ was released from Nitr-5 by flash photolysis, at which point channel activity was transiently suppressed. Similar effects were seen when db-cAMP was used instead of glucagon.These results support the view that glucagon and other cAMP-generating agonists enhance glucose-induced β-cell electrical activity through a Ca2+/calmodulin dependent-closure of K(ATP) channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002329900465
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  • 3
    Electronic Resource
    Electronic Resource
    Phylogenetic and ontogenetic study of neuropeptide Y-containing nerves in the liver (1994)
    Springer
    Journal of molecular histology 26 (1994), S. 453-459 
    Details
    ISSN: 1573-6865
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The distribution of neuropeptide Y was investigated by light and electron microscopic immunohistochemistry in the liver of various vertebrates including the eel, carp, bullfrog, turtle, chicken, mouse, rat, guinea-pig, dog, monkey and human. The ontogenetic development of neuropeptide Y was also studied in the mouse liver. In all species examined except the eel, neuropeptide Y-like immunoreactivity was detected in nerve fibres. In the carp, bullfrog, turtle, chicken, mouse and rat, positive fibres were distributed around the wall of hepatic vessels and the bile duct of the Glisson's sheath. The density of the positive fibres increased with evolution. On the other hand, in the guinea-pig, dog, monkey and human, numerous neuropeptide Y-positive fibres were observed not only in the Glisson's sheath but also in the liver parenchyma. Positive fibres formed a dense network to surround hepatocytes. The present immunoelectron microscopic study has confirmed that neuropeptide Y-positive terminals are closely apposing to hepatocytes. Ontogenetically, neuropeptide Y-positive fibres were first found in embryonic liver of 19-day-old mice. Positive fibres increased with age and the highest peak was seen one week after birth. This ontogenetic pattern has suggested that neuropeptide Y plays a certain role in developing liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00160059
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    Paper (German National Licenses)
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