Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: DEMBIŃSKI
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Tytuł oryginału: The influence of epidermal growth factor on the course of ischemia-reperfusion induced pancreatitis in rats.
Autorzy: Tomaszewska R., Dembiński A[rtur], Warzecha Z., Ceranowicz P., Konturek S[tanisław] J., Stachura J.
Źródło: J. Physiol. Pharmacol. 2002: 53 (2) s.183-198, il., tab., bibliogr. 49 poz.
Sygnatura GBL: 302,092

Hasła klasyfikacyjne GBL:
  • gastroenterologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Acute pancreatitis is accompanied by the enhanced expression of EGF in the pancreas and the administration of EGF was found to exhibit the beneficial efect on edematous cerulein-induced pancreatitis. Therefore, we decided to determine the influence of EGF on necro-hemorrhagic pancreatitis induced by ischaemia and reperfusion (I/R). Acute pancreatitis ws induced in rats by rectricting the pancreatic blood flow (PBF) in the inferior splenic artery for 30 min using microvascular clips. EGF was administered three times daily (10ć/kg per dose s.c.) starting immediately after the clips removal. Rats were sacrificied on day 1,3,5,10 and 21 following ischemia. PBF was measured using a laser Doppler flowmeter. Morphological signs of pancreatitis, as well as the levels of plasma amylase, lipase, interleukin-1á and interleukin-10 concentration and pancreatic cell proliferation were examined. Results: Ischemia with reperfusion caused necro-hemorrhagic pancreatitis with a histological and biochemical maifestation of pancreatic damage, followed by a spontaneous regeneration. The administration of EGF caused the reduction in the histological signs of pancreatic damage, such as necrosis, edema and leukocyte infiltration, and accelerated the pancreatic repair. Also, EGF treatment significantly attenuated the reduction in pancreatic blood flow and DNA syntehsis. The activity of plasma amylase and lipase, as well as plasma interleukin-1á and interleukin-10 concentrations were decreased in EGF treated animals. Conclusions: ...


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    Tytuł oryginału: Influence of leptin administration on the course of acute ischemic pancreatitis.
    Autorzy: Warzecha Z., Dembiński A[rtur], Ceranowicz P., Jaworek J., Konturek P. C., Dembiński M., Bilski J., Konturek S[tanisław] J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 2) s.775-790, il., tab., bibliogr. 57 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • gastroenterologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • szczury
  • płeć męska

    Streszczenie angielskie: Leptin is involved in the regulation of food intake and previous studied have shown that leptin affects the inflammatory response in various tissues. The objective of this study was to examine the influence of leptin administration on the development and the course of acute ischemic pancreatitis. Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion. Leptin was administered three times daily at the dose 10 or 50 ćg/kg. Animals were sacrificed 1, 3, 5, 10 and 21 days after removal of vascular clips. Administration of leptin reduced development of pancreatic damage and accelerated pancreatic regeneration what was manifested by the improvement of pancreatic histology, the decrease in serum lipase and amylase activity, and the reduction in serum interleukin-1á concentration. Also, treatment with leptin caused the increase in the pancreatic blood flow and pancreatic DNA synthesis. Leptin administration was without effect on serum interleukin-10 concentration. Leptin at the dose 50 ć/kg was more effective than 10 ćg/kg. We conclude that leptin reduces the pancreatic damage in the course of ischemic pancreatitis and accelerates the pancreatic tissue repair. The beneficial effects of leptin appear to be dependent on the improvement of pancreatic blood flow, the increase in pancreatic cell growth, and the limitation of pro-inflammatory interleukin-1á release.

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