Journals / Turkish Journal of Medical Sciences / 2006 / Cilt: 36 - Sayı: 4

The Effect of Erythropoietin in Acute Pancreatitis: An Experimental Study

Pages
215–221
Publication Date
2022-11-05
DOI
—
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Conclusions: The results we have obtained demonstrate that more controlled models (employing low rates of sodium taurocholate or edematous pancreatitis) are necessary to better investigate the efficacy of EPO.

📌 3 Key Takeaways

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Objective & Hypothesis:Background: Although the pathogenesis of acute pancreatitis is not clearly known, the most frequently mentioned factors are proinflammatory cytokines and nitric oxide (NO), which is stimulated by bacterial endotoxins.
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Key Findings & Data:Materials and Methods: 60 Wistar Albino rats were divided into 4 groups as follows: laparotomy (I), pancreatitis (II), pancreatitis + simultaneous application of EPO (III) and finally pancreatitis + administration of EPO after 3 hours (IV).
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Conclusion & Impact:Conclusions: The results we have obtained demonstrate that more controlled models (employing low rates of sodium taurocholate or edematous pancreatitis) are necessary to better investigate the efficacy of EPO.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Acute pancreatitis · experimental model · histopathology

Abstract

Background: Although the pathogenesis of acute pancreatitis is not clearly known, the most frequently mentioned factors are proinflammatory cytokines and nitric oxide (NO), which is stimulated by bacterial endotoxins. The relationship of erythropoietin (EPO), which is an erythroid line growth hormone, with proinflammatory cytokines and NO is also not clear. EPO has a well-known general tissue protective effect, yet its role in an inflammatory presentation like that of acute pancreatitis has not been investigated and documented. Therefore, the aim of this study was to investigate the role of EPO in acute pancreatitis. Materials and Methods: 60 Wistar Albino rats were divided into 4 groups as follows: laparotomy (I), pancreatitis (II), pancreatitis + simultaneous application of EPO (III) and finally pancreatitis + administration of EPO after 3 hours (IV). The groups were further separated to subgroups by sacrificing the animals at 3, 6 and 24 hours. Pancreatitis was induced by injecting 4.5% sodium (Na)-taurocholate (0.1 ml / 100 g) into the pancreatic canal. Leukocyte counts and serum amylase and C-reactive protein (CRP) levels were measured. Histopathological changes of the pancreas were evaluated according to Spormann scores. Results: EPO was shown to increase leukocyte counts in the early phase (P < 0.05) though the effect diminished in time. It also had an increasing effect on amylase in the early hours (P < 0.005), but the difference between the groups disappeared in the following hours. No effect was demonstrated on serum CRP. Pancreatic tissue revealed moderate degree of pancreatitis in group III sacrificed at 6 hours and in group IV evaluated at 6 and 24 hours. Despite the absence of a difference in the numerical analysis of Spormann scoring (P > 0.05), moderate pancreatitis developed in the group receiving EPO. Conclusions: The results we have obtained demonstrate that more controlled models (employing low rates of sodium taurocholate or edematous pancreatitis) are necessary to better investigate the efficacy of EPO.

Özet

Background: Although the pathogenesis of acute pancreatitis is not clearly known, the most frequently mentioned factors are proinflammatory cytokines and nitric oxide (NO), which is stimulated by bacterial endotoxins. The relationship of erythropoietin (EPO), which is an erythroid line growth hormone, with proinflammatory cytokines and NO is also not clear. EPO has a well-known general tissue protective effect, yet its role in an inflammatory presentation like that of acute pancreatitis has not been investigated and documented. Therefore, the aim of this study was to investigate the role of EPO in acute pancreatitis. Materials and Methods: 60 Wistar Albino rats were divided into 4 groups as follows: laparotomy (I), pancreatitis (II), pancreatitis + simultaneous application of EPO (III) and finally pancreatitis + administration of EPO after 3 hours (IV). The groups were further separated to subgroups by sacrificing the animals at 3, 6 and 24 hours. Pancreatitis was induced by injecting 4.5% sodium (Na)-taurocholate (0.1 ml / 100 g) into the pancreatic canal. Leukocyte counts and serum amylase and C-reactive protein (CRP) levels were measured. Histopathological changes of the pancreas were evaluated according to Spormann scores. Results: EPO was shown to increase leukocyte counts in the early phase (P < 0.05) though the effect diminished in time. It also had an increasing effect on amylase in the early hours (P < 0.005), but the difference between the groups disappeared in the following hours. No effect was demonstrated on serum CRP. Pancreatic tissue revealed moderate degree of pancreatitis in group III sacrificed at 6 hours and in group IV evaluated at 6 and 24 hours. Despite the absence of a difference in the numerical analysis of Spormann scoring (P > 0.05), moderate pancreatitis developed in the group receiving EPO. Conclusions: The results we have obtained demonstrate that more controlled models (employing low rates of sodium taurocholate or edematous pancreatitis) are necessary to better investigate the efficacy of EPO.

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Cite This Article

COŞKUN, F., KAHRAMANSOY, N., DÜZGÜN, P. A., ÖZMEN, M. M., SEÇKİN, S., ÖZGEDİK, B. M. (2022). The Effect of Erythropoietin in Acute Pancreatitis: An Experimental Study. Turkish Journal of Medical Sciences, Cilt: 36 - Sayı: 4, 215–221. https://ajindex.com/articles/611928

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References (8)

  1. Grady T, Liang P, Ernst SA, Logsdon CD. Chemokine gene expression in rat pancreatic acinar cells is an early event associated with acute pancreatitis. Gastroenterology. 1997; 113(6): 1966- 1975.
  2. Norman J, Franz M, Messina J, Riker A, Fabri PJ, Rosemurgy AS, Gower WR Jr. Interleukin-1 receptor antagonist decreases severity of experimental acute pancreatitis. Surgery. 1995; 117(6): 648-655. 9. Scholmerich J. Interleukins in acute pancreatitis. Scand J Gastroenterol Suppl. 1996; 219: 37-42.
  3. Rau B, Poch B, Gansauge F, Bauer A, Nussler AK, Nevalainen T et al. Pathophysiologic role of oxygen free radicals in acute pancreatitis: initiating event or mediator of tissue damage? Ann Surg. 2000; 231(3): 352-360.
  4. Rau B, Paszkowski A, Lillich S, Baumgart K, Moller P, Beger HG. Differential effects of caspase-1/interleukin-1 beta-converting enzyme on acinar cell necrosis and apoptosis in severe acute experimental pancreatitis. Lab Invest. 2001 Jul; 81(7): 1001- 1013. Gukovskaya AS, Gukovsky I, Zaninovic V, Song M, Sandoval D, Gukovsky S et al. Pancreatic acinar cells produce, release, and respond to tumor necrosis factor-alpha. Role in regulating cell death and pancreatitis. J Clin Invest. 1997; 1; 100(7): 1853- 1862. Akimoto T, Kusano E, Fujita N, Okada K, Saito O, Ono S et al. Erythropoietin modulates angiotensin II- or noradrenaline- induced Ca (2+) mobilization in cultured rat vascular smooth- muscle cells. Nephrol Dial Transplant. 2001; 16(3): 491-499.
  5. Siren AL, Fratelli M, Brines M, Goemans C, Casagrande S, Lewczuk P, Keenan S, Gleiter C, Pasquali C, Capobianco A, Mennini T, Heumann R, Cerami A, Ehrenreich H, Ghezzi P. Erythropoietin prevents neuronal apoptosis after cerebral ischemia and metabolic stress. Proc Natl Acad Sci U S A. 2001; 27; 98(7): 4044-4049. Epub 2001 Mar 20. Sakanaka M, Wen TC, Matsuda S, Masuda S, Morishita E, Nagao M, Sasaki R. In vivo evidence that erythropoietin protects neurons from ischemic damage. Proc Natl Acad Sci USA. 1998; 14; 95(8): 4635-4640.
  6. Rau B, Bauer A, Wang A, Gansauge F, Wiedenbach H. Modulation of endogenous nitric oxide synthase in experimental acute pancreatitis: role of anti-ICAM-1 and oxygen free radical scavengers. Ann Surg. 2001; 233(2): 195-203. al-Mufti RA, Williamson RC. Experimental models of pancreatitis. Ann Acad Med Singapore. 1999; 28(1): 133-140.
  7. Weber A, Friess H, Sill U, Buchler M. The closed duodenal loop technique. Eur Surg Res. 1992; 24 Suppl 1: 24-28.
  8. Nevalainen TJ, Aho HJ. Standards of morphological eval