Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: TETICH
Liczba odnalezionych rekordów: 3



Przejście do opcji zmiany formatu | Wyświetlenie wyników w wersji do druku

1/3

Tytuł oryginału: Chlorpromazine inhibits the glucocorticoid receptor-mediated gene transcription in a calcium-dependent manner.
Autorzy: Basta-Kaim A., Budziszewska B., Jaworska-Feil L., Tetich M., Leśkiewicz M., Kubera M., Lasoń W.
Źródło: Neuropharmacology 2002: 43 (6) s.1035-1043, il., bibliogr. [36] poz.
Sygnatura GBL: 305,141

Hasła klasyfikacyjne GBL:
  • pediatria
  • neurologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy

    Streszczenie angielskie: Antipsychotic drugs can modulate transcription factors ansd also nuclear receptors, but their action on glucocorticoid receptors (GR)-members of the steroid/thyroid hormone receptor family has been studied so far. In the present study we investigated effects of various antipsychotics on the glucocorticol-mediated gene transcription in fibroplast cells, stably tranfected with a mouse mammary tumor virus promoter (LMCAT cells). Chlorpromazine (3-100 ćM) inhibited the corticosterone-induced gene transcription in a concentration- and time-dependent manner. Clozapine showed a similar, but less potent effect, while haloperiod acted only in high concentrations, and other antipsychotics drugs (sulpiride, raclopride, remoxipride) were without any effect. It was also found that a phorbol ester (an activator of protein kinase C (PKC) and A-23187 (Ca2+-ionophore) attenuated the inhibitory effect of chloropromazine on the GR-induced gene transcription. An antagonist of the L-type Ca2+ channel, as an inhibitor of phospholipase C (PLC) inhibited the corticosterone-induced gene transcription, but had no effect on the chlorpromazine-induced changes. The involvement of a PKC/LC pathway in the chlorpromazine action was confirmed by Western blot analysis showed that the drug in question decreased the PLC-á1 protein level, and to a lesser extent that of the PKC-ŕ protein in LMCAT cells. The aferomentioned data suggest that inhibition of the glucorticosteroid-induced gene transcription by chlorpromazine and clozapine may be a mechanism by which these drugs block some effects induced...


    2/3

    Tytuł oryginału: The effect of amphetamine sensitization on mouse immunoreactivity.
    Autorzy: Kubera M., Filip M., Basta-Kaim A., Nowak E., Budziszewska B., Tetich M., Holan V., Korzeniak B., Przegaliński E.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (2) s.233-242, il., tab., bibliogr. 24 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • toksykologia
  • immunologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • płeć męska

    Streszczenie angielskie: Recent studies indicate a role of the immune system in the behavioral effects of amphetamine in rodents. In the present study we attempted to find a connection between the behavioral changes induced by repeated, intermittent administration of amphetamine and some immunological consequences of sensitization to amphetamine in mice. Male Albino Swiss mice were treated repeatedly (for 5 days) with amphetamine (1 mg/kg, i.p.). On day 9, they received a challenge dose of amphetamine (1 mg/kg). Acute administration of amphetamine increased their locomotor activity by ca. 40 p.c. In animals treated repeatedly with amphetamine, the challenge dose of the psychostimulant induced behavioral sensitization, i.e. the higher locomotor activation as compared with that after its first administration to mice. Immune functions were evaluated by the ability of splenocytes to proliferate and to produce cytokines such as interferon ç(IFN-ç), interleukin (IL)-4 and IL-10. Acute amphetamine administration significantly decreased, by ca. 30 p.c. and 25 p.c., the proliferation of splenocytes in response to an optimal and a suboptimal dose of concanavalin A (Con A), respectively, and increased their ability to produce IL-4. Chronic intermitent treatment with amphetamine significantly decreased, by ca. 65 p.c. and 50 p.c., the proliferative response of T cells to an optimal and a suboptimal dose of Con A, respectively, and diminished by 20 p.c. the metabolic activity of splenocytes. The above data showed that both acute and chronic amphetamine ...


    3/3

    Tytuł oryginału: Effect of antidepressant drugs on the human corticotropin-releasing-hormone gene promoter activity in neuro-2A cells.
    Autorzy: Budziszewska Bogusława, Jaworska-Feil Lucylla, Tetich Małgorzata, Basta-Kaim Agnieszka, Kubera Marta, Leśkiewicz Monika, Lasoń Władysław
    Źródło: Pol. J. Pharmacol. 2002: 54 (6) s.711-716, il., bibliogr. 16 poz.
    Sygnatura GBL: 313,156

    Hasła klasyfikacyjne GBL:
  • genetyka
  • endokrynologia
  • farmacja

    Typ dokumentu:
  • praca doświadczalna
  • komunikat
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie

    Streszczenie angielskie: In order to test if antidepressant drugs can directly influence corticotropin-releasing hormone (CRH) gene expression, their effect on CRH gene promoter activity was evaluated in neuro-2A cells stably transfected with a human CRH - chloramphenicol acetyl-transferase plasmid. Forskolin (an activator of adenylate cyclase), but not phorbol 12-myristate 13-acetate (an activator of protein kinase C), ca. 3-fold increased reporter gene activity, which confirms the critical role of the cAMP-responsive element in regulation of the CRH gene. Imipramine and fluoxetine present in the medium for 5 days, in a concentration-dependent manner (3-30 ćM) inhibited the basal acitivity of CRH gene promoter, while tianeptine was inactive. The obtained results indicate that inhibition of the human CHR gene promoter activity by imipramine and fluoxetine, but not tianeptine, may play a role in mechanism by which the former drugs attenuate HPA axis activity.

    stosując format: