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Tytuł oryginału: Agonists of peroxisome-proliferator activated receptor-ŕ (Clofibrate and WY14643) reduce renal ischemia/reperfusion injury in the rat.
Autorzy: Sivarajah Ahila, Chatterjee Prabal K., Hattori Yoshiyuki, Brown Paul A. J., Stewart Keith N., Todorovic Zoran, Mota-Filipe Helder, Thiemermann Christoph
Źródło: Med. Sci. Monitor 2002: 8 (12) s.BR532-BR539, il., tab., bibliogr. 37 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • farmacja
  • nefrologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Background: The aim of this study was to investigate the effects of peroxisome-proliferator activated receptor-ŕ (PPAR-ŕ) agonsits, clofibrate and WY 14643 on the renal dysfunction and injury caused by bilateral ischemia/reperfusion (I/R) of rat kidneys in vivo. Material/Methods: Male Wistar were randomized with sodium thiopentone (120 mg/kg i.v.) and subjected to bilateral renal ischemia (45 min) followed by reperfusion (6 h). Serum and urinary biochemical indicators of renal dysfunction and injury were meausured; serum creatine (sCr, glomerular dysfunction), fractional excretion of Na+ (FE NA, tubular dysfunction), and urinary N-acetyl-á-D-glucosaminidase (uNAG, tubular injury). Additionally, renal sections were used for histological grading of renal injury and for RT-PCR analysis of the expression of PPAR-isoforms in kidneys obtained from rats prior to or after I/R. In addition, expression of intercellular adhesion molecule-1 (ICAM-1) was determined using Northern blot analysis. Results: Using RT-PCR we document here the expression of PPAR-ŕ, PPAR-á and PPAR-ç1 (but not PPAR-ç2) in the kidney of the rat. I/R resulted in the down-regulation of PPAR-ŕ without modulation of any other PPAR. Clofibrate and WY 14643 significantly reduced the increases in sCr, FE NA and uNAG caused by renal I/R, indicating attenuation of renal dysfunction and injury. Expression of ICAM-1 caused by I/R of the kidney was not modulated by PPAR-ŕ agonists. Conclusions: We show here that (i) renal I/R results in the down-regulation of PPAR-ŕ in the kidney, and (ii) that the PPAR-ŕ agonists...

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