Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

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Tytuł oryginału: Superoxide dismutase mimetic with catalase activity, EUK-134, attenuates the multiple organ injury and dysfunction caused by endotoxin in the rat.
Autorzy: Villa Bianca Roberta d'Emanuele di, Wayman Nicol S., McDonald Michelle C., Pinto Aldo, Sharpe Martyn A., Chatterjee Prabal K., Thiemermann Christoph
Źródło: Med. Sci. Monitor 2002: 8 (1) s.BR1-BR7, il., tab., bibliogr. 33 poz.
Sygnatura GBL: 313,278

Hasła klasyfikacyjne GBL:
  • farmacja
  • traumatologia i ortopedia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury

    Streszczenie angielskie: Reactive oxygen species contribute to the multiple organ failure shock. Here we investigate the effects of a salen-manganese complex, which exhibits both superoxide dismutase and catalase activity (EUK-134), on the circulatory failure and the renal and liver injury and dysfunction caused by endotoxin in the anaesthetised (thiopentone, 120 mg/kg) rat. Male Wistar rats were anaesthetised with hiopentone sodium (120 kg i.p.) and instrumented for the measurements of systemic haemodynamics. Animals received lipopolysaccharide (LPS, E. coli, 6 mg/kg i.v.) or saline and were treated with either EUK-134 (0.3 or 1 mg/kg bolus injection folloowed by an infusion of 0.3 or 1 mg/kg/h) or its vehicle (saline). After 6 h of endotoxaemia, blood was taken to evaluate biochemical parameters of organ injury and dysfunction. All data are mean ń s.e. mean of n observations. Statisstical comparisons were made with a ANOVA followed by Dunner's test for mulitiple comparisons. Endotoxaemia for 6 h caused hypotension, renal dysfunction, liver injury, skeletal-muscle injury and pancreatic injury. Treatment of rats with EUK-134 attenuated the reanl dysfynction as well as the liver and skeletal muscle injury (but not the pancreatic injury) caused by endotoxin. Thus, an enhanced formation of reactive oxygen species importantly contribute to the organ injury and dysfunction associated wtih endotoxic shock. We propose that small molecules, which have the catalytic activity of both superoxide dismutase and catalase, may represent a novel therapeutic approach for the therapy of endotoxic shock.

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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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