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Tytuł oryginału: Mechanisms of delayed preconditioning with A1 adenosine receptor activation in porcine coronary smooth muscle cells.
Autorzy: Neyeem Mohammed A., Mustafa S. Jamal
Źródło: Pol. J. Pharmacol. 2002: 54 (5) s.443-453, il., bibliogr. 49 poz.
Sygnatura GBL: 313,156

Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • Świnie

    Streszczenie angielskie: This study examined the hypothesis that the activation of A1 adenosine receptor (A1AR) induces delayed cellular protection (DCP) in porcine coronary smooth muscle cells (PCSMC). The following groups of cultured PCSMC, subjected to simulated ischemia (SI) at 20 h were studied: (a) SI: with ischemia alone; (b) A1AR agonist chloro-N6-cyclopentyl adenosine (CCPA: CCPA (1 ćM) alone; (c) CCPA + PKC inhibitor chelerythrine chloride (CCL): CCPA and 1 ćM CCL; (d) CCPA + iNOS inhibitor S-methylthiourea (SMT): CCPA and 100 nM SMT; (e) CCPA + KATP channel blocker Glibaenclamide (Glb): CCPA adn 50 ćM Glb; (f) CCPA + mitochondrial KATP channel blocker 5-hydroxydecanoate (5-HD): CCPA and 100 ćM of 5-HD; (g) CCPA + A1AR antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX): CCPA and 1ćM DPCPX. The release of LDH into the medium as well as the amount of LDH remaining in the cells was used as a marker of cellular injury and cell viability. Up-regulation of A1AR, î-PKC, iNOS and HSP 72i was detected through Western blot analysis. The cellular resistance (LDH remaining in the cells) acquired by PCSMC due to CCPA (59.42 ń 1.57) was significantly blocked by CCL; 39.30 ń 2.03; SMT: 41.37 ń 1.98; Glb: 47.24 ń 1.31; 5-HD: 47.69 ń 1.40 and DPCPX: 42.92 ń 0.79. CCPA increased the expression of A1AR (1.30 fold), î-PKC (1.20 fold), iNOS (1.50 fold), and HSP 72i (1.70 fold) compared to the controls. CCPA-induced upregulation of A1AR, î-PKC, iNOS, HSP 72i, and the opening of both mitochondrial and sercolemmal KATP channels may possibly participate in signaling cascade. Our study suggests that A1AR activation up-regulates iNOS, HSP 72i via î-PKC signaling pathway to active both mitochondrial and sarcolemmal KATP channels for cellular protection against SI in the acultured PCSMC.

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