Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: SLOMIANY A
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Tytuł oryginału: Activation of peroxisome proliferator-activated receptor ç suppresses inducible cyclooxygenase and nitric oxide synthase during oral mucosal ulcer healing.
Autorzy: Slomiany B. L., Slomiany A.
Źródło: J. Physiol. Pharmacol. 2002: 53 (2) s.159-169, il., bibliogr. 44 poz.
Sygnatura GBL: 302,092

Hasła klasyfikacyjne GBL:
  • stomatologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Background: Peroxisome proliferator-activated receptor-ç (PPARç) is a ligand-dependent transcription factor, belonging to the steroid hormone receptor family, known to play a pivotal role in the resolution of inflammation. In this study, we investigated the efect of a specific PPAR-ç ligand, ciglitazone, on the course of buccal mucosal ulcer healing by analyzing mucosal activity of inducible nitric oxide synthase (NOS-2) and the expression cyclooxygenases (COX-1 an dCOX-2) responsible for prostaglandin (PG) generation. Methods: Groups of rats with experimentally induced buccal mucosal ulcers were administered twice daily for up to 10 days with ciglitazone at 5, 10, and 15 mg/kg or the vehicle, and their mucosal tissue subjected to assessment of ulcer healing rate and biochemical measurements. Results: The ulcer onset, characterized by up-regulation of NOS-2 and COX-2 protein expression, was reflected in a marked increase in the mucosal PGE2 generation and NOS-2 activity, whereas healing was accompanied by a drop in PGE2 and nOS-2 activity, and a decrease in COX-2 and NOS-2 protein expression. The mucosal expression of COX-1 protein, however, remained unchanged. Administration of ciglitazone led to a significant dose-dependent acceleration in the mucosal reduction of PGE2 generation and NOS-2 activity, and produced a marked decline in COX-2 and NOS-2 protein expression, but the rate of ulcer healing and the expression of COX-1 protein remained unaffected. Conclusions: Our findings thus suggest that the ...

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    Tytuł oryginału: Screening and modulation of extracellular signals by mucous barrier. Serum glycosylphosphatidylinositol phospholipase D (GPI-PLD) releases protective mucous barrier from oral mucosa.
    Autorzy: Slomiany A., Nishikawa H., Slomiany B. L.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (1) s.21-38, il., bibliogr. 52 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • stomatologia
  • toksykologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Bacground: Performance of musocal epithelial barrier is modified by numerous agents that exert effects on mucin- Mucin Binding Protein (MBP) complex. The aim of the studies described was to determine the nature of the damage or modification of oral mucous barrier by the short-term exposure to ethanol. Methods: Culture of rat buccal mucosa in the presence of ethanol and [3H]-labeled proline and palmitate revealed decrease in MBP synthesis and the release of MBP to the medium. The radioscanning of the samples prepared from the culture medium and the apical epithelial membranes subjected to SDSPAGE and western blotting disclosed that the released, water soluble 97 Da MBP glycopeptide was lebeled with proline and palmitate. When the experiments were conducted in the presence of 5mM EDTA, the GPI-PLD inhibitor, the majority of radiolabeled MBP remained in the membrane-bound from and was extractable with Triton X-114. The results on the purified GPI-linked MBP degradation by serum enzyme, by the saliva containing serum transudate, and the suppression of the process by inclusion of GPI-PLD-specific inhibitor support our contention that membrane MBP is released to medium by GPI-PLD-like activity. Results: The release of MBP from apical epithelial surfaces was induced by depletion of mucin and the presence of serum-derived GPI-PLD in the tissue homogenate. Strong likelihood exists that under in situ conditions ethanol-induced transudation of serum to saliva provides the vehicle for the transfer of GPI-PLD activity to salivary contents...

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    Tytuł oryginału: Nitric oxide interferes with salivary mucin synthesis: involvement of ERK and p38 mitogen-activated protein kinase.
    Autorzy: Slomiany B. L., Slomiany A.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (3) s.325-336, il., bibliogr. 31 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • stomatologia

    Typ dokumentu:
  • tytuł obcojęzyczny
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Background: Nitric oxide (NO), a pluripotent molecule, is an important biological messenger that plays a role in the regulation of tissue homeostasis and pathophysiological processes. Methods: Using sublingual salivary gland acinar cells in culture, we investigated the effect of NO on mucus glycoprotein synthesis, apoptotic processes, and the involvement of extracellular signal-regulated kinase (ERK) and p38 mitogen activated protein kinase (MAPK). Results: Exposure of the acinar cells to NO donor led to a dose-dependent decrease (up to 42.8 p.c.) in mucus glycoprotein synthesis, and this effect of NO was accompanied by a marked increase in capase-3 activity and apoptosis. Inhibition of ERK with PD98059 accelerated (up to 35.4 p.c.) the NO-induced decrease in the glycoprotein synthesis, and cause further enhancement in caspase-3 (up to 27.2 p.c.) activity and apoptosis (64.9 p.c.). On the other hand, blockade of p38 kinase with SB203580 produced a dose-dependent reversal (up to 42 p.c.) in the NO-induced reduction in the glycoprotein syntehsis, and substantially countered the NO-induced increased in capase-3 activity (by 62.8 p.c.) and apoptosis (by 57.6 p.c.). Moreover, caspase-3 inhibitor, Ac-DEVD-CHO, not only blocked the NO-induced in caspase-3 activity but also produced an increase in the glycoprotein synthesis. Conclusions: Together, our data indicate that the modulatory influence of NO on salivary mucin synthesis is closely linked to ERK and p38 protein kinase activation, in conjunction with caspase-3 activation and apoptosis.

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