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The Investigation Effects of Enalapril and Losartan on The Renal Tissues of The Experimental Diabetic Rats

Year 2011, Volume: 16 Issue: 2, 46 - 50, 01.04.2011

Mehmet Murat Doğan Emir Dönder Tuncay Kuloğlu Dürrin Özlem Dabak

Abstract

Objective: The aim of this study was to determine the effects of Enalapril and Losartan on renal tissues of Streptozocin(STZ)-induced diabetic rats. Materials and Methods: 28 Wistar rats were used in this study. All rats were divided into 4 groups as control group (n=7), diabetic group (n=7), DM+ Enalapril (n=7) and DM+ Losartan group (n=7). 50 mg/kg STZ administered intraperitoneally to diabetic, DM+ Enalapril, DM+ Losartan groups. Five mg/kg/day Enalapril and 10 mg/kg/day Losartan were orally administered to treatment group from the begining of the diabetes. At the end of fourth week all rats were decapitated and renal tissues were removed. Tissue samples were processed by using routine paraffin techniques. Paraffin sections were stained with periodic-acid-schiff (PAS). Results: Glomerules and tubules of control group were normal. In diabetic group; narrowing in Bowman spaces of some glomeruli, mesangial matrix enlargement and tubular dilatations were determined. Additionally; loosing of brush like edges of tubular epithelial cells, falling of the cells to the lumene of tubules, thickening of tubular basement membrane and Armanni-Ebstein lesions were determined. The histologic appearance of DM+ Enalapril and DM+ Losartan groups were similar. There were narrowing in Bowman spaces, mesangial matrix enlargement and thickening of tubular basement membranes. Tubular dilatation and Armanni-Ebstein lesions were less remarkable than diabetic group. Loosing of brush like edges of tubular epithelial cells were decreased. Conclusıons: It was determined that enalapril and losartan have healing effects on the kidney tissues of STZ- induced diabetic rats.

Keywords

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References

  • 1. Powers AC. Diabetes Mellitus. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, (eds). Harrison’s principles of Internal Medicine. 16th ed. McGraw Hill, 2005; 2152- 2180.
  • 2. Kahn CR, Weir GC, King GL, Jacobson AM, Moses AC, Smith RJ. Joslin’s Diabetes Mellitus. Fourteenth edition. Boston: Lippincott Williams and Wilkins, 2005; 331–338.
  • 3. Rahimi R, Nikfar S, Larijani B, Abdollahi M. A review on the role of antioxidants in the management of diabetes and its complications. Biomed Pharmacother 2005; 59: 365–373.
  • 4. Cooper ME. Interaction of metabolic and hemodynamic factors in mediating experimental diabetic nephropathy. Diabetologia 2001; 44: 1957–1972.
  • 5. Taniyama Y, Griendling KK. Reactive oxygen species in the vasculature: Molecular and cellular mechanisms. Hypertension 2003, 42: 1075–1081.
  • 6. Touyz RM. Reactive oxygen species and angiotensin II signaling in vascular cells implications in cardiovascular disease. Braz J Med Biol Res 2004; 37: 1263–1273.
  • 7. Touyz RM, Schiffrin EL. Ang II-stimulated superoxide production is mediated via phospholipase D in human vascular smooth muscle cells. Hypertension 1999; 34: 976–982.
  • 8. Onozato ML, Tojo A, Goto A, Fujita T, Wilcox CS. Oxidative stress and nitric oxide synthase in rat diabetic nephropathy: effects of ACEI and ARB. Kidney Int 2002; 61: 186 -194.
  • 9. Berry C, Anderson N, Kirk AJ, Dominiczak AF, McMurray JJ. Renin angiotensin system inhibition is associated with reduced free radical concentrations in arteries of patients with coronary heart disease. Heart 2001; 86: 217–220.
  • 10. Johansen JS, Harris AK, Rychly DJ and Ergul A. Oxidative stress and the use of antioxidants in diabetes: Linking basic science to clinical practice. Cardiovascular Diabetology 2005; 4: 5.
  • 11. Fan Q, Liao J, Kobayashi M, et al. Candesartan reduced advanced glycation end-products 56 accumulation and diminished nitro-oxidative stress in type 2 diabetic KK/Ta mice. Nephrol Dial Transplant 2004; 19: 3012–3020.
  • 12. Kumar V, Cotran RS, Robbins SL. Temel Patoloji, Prof. Dr. Uğur Çevikbaş (ed). s:511–517. 6. Baskı, Nobel Tıp Kitabevi, İstanbul, 2000.
  • 13. Ronco C, La Greca G. Vitamin E bonded membrane, a further step in dialysis optizimation. Contrib Nephrol 1999; 127: 1– 31.
  • 14. Sies H. Oxidants and antioxidants. Exp Physiol 1997; 82: 291- 295.
  • 15. Altan N, Dinçel AS, Koca C, Diabetes Mellitus ve Oksidatif Stres Türk Biyokimya Dergisi 2006; 31; 51–56.
  • 16. Tesfamariam B. Free radicals in diabetic endothelial dysfunction. Free Radic Biol Med 1994;16: 383–391.
  • 17. Komers R, Lindsley JN, Oyama TT, Allison KM, Anderson S. Role of neuronal nitric oxide synthase (NOS1) in the pathogenesis of renal hemodynamic changes in diabetes. Am J Physiol Renal Physiol 2000; 279: 573–583.
  • 18. Esposito C, Liu ZH, Striker GE, et al. Inhibition of diabetic nephropathy by a GH antagonist: A molecular analysis. Kidney Int 1996; 50: 506–514.
  • 19. Lundbaek K, Christensen NJ, Jensen VA, et al. Diabetes, diabetic angiopathy, and growth hormone. Lancet 1970; 2: 131–133.
  • 20. Osterby R, Asplund J, Bangstad HJ, et al. Neovascularization at the vascular pole region in diabetic glomerulopathy. Nephrol Dial Transplant 1999; 14: 348–352.
  • 21. Cortes P, Dumler F, Goldman J, Levin NW. Relationship between renal function and metabolic alterations in early streptozocin-induced diabetes in rats. Diabetes 1987; 36: 80– 87.
  • 22. Sanai T, Sobka T, Johnson T, et al. Expression of cytoskeletal proteins during the course of experimental diabetic nephropathy. Diabetologia 2000; 43: 91–100.
  • 23. Tucker BJ, Collins RC, Ziegler MG, Blantz RC. Disassociation between glomerular hyperfiltration and extracellular volume in diabetic rats. Kidney Int 1991; 39: 1176–1183.
  • 24. New JP, Canavan JP, Flyvbjerg A, Hamon G, Bilous RW, Marshall SM. Renal enlargement and insulin-like growth factor–1 accumulation in the Wistar rat model of experimental diabetes is not prevented by angiotensin converting enzyme inhibition. Diabetologia 1996; 39: 166–171.
  • 25. Büyükdevrim AS, Büyükbeşe MA, Davutoğlu M. Diabetik nefropati. Klinik moleküler patogenez klasik ve moleküler tedavi. İstanbul: Turgut yayıncılık, 2005; 432–529, 136–342.
  • 26. De Cavanagh EMV, Inserra F, Toblli J, Stella I, Fraga C.G and Ferder L. Enalapril Attenuates Oxidative Stress in Diabetic Rats. Hypertension 2001; 38: 1130–1136.
  • 27. Dönmez S. Deneysel Diabetik Nefropatide İrbesartan ve Antioksidan Tedavilerin Karşılaştırılması, Uzmanlık Tezi 2008; 46–58.

Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan'ın Etkilerinin İncelenmesi

Year 2011, Volume: 16 Issue: 2, 46 - 50, 01.04.2011

Mehmet Murat Doğan Emir Dönder Tuncay Kuloğlu Dürrin Özlem Dabak

Abstract

Amaç: Bu çalışmada, streptozotosin (STZ) ile deneysel olarak diyabet oluşturulan sıçanların böbrek dokusunda, Enalapril ve Losartan'ın iyileştirici etkilerinin incelenmesi amaçlandı. Gereç ve Yöntem: Çalışmada 28 adet erişkin, Wistar cinsi sıçan kullanıldı. Deney hayvanları Kontrol grubu (n=7), diyabetik (DM) grup (n=7), DM+ Enalapril (n=7) ve DM+ Losartan (n=7) olmak üzere dört gruba ayrıldı. Diyabetik, DM+ Enalapril ve DM+ Losartan gruplarına 50 mg/kg tek doz STZ intraperitoneal olarak uygulandı. Tedavi gruplarındaki sıçanlara diyabetin başlangıcından itibaren 5 mg/kg/gün Enalapril ve 10 mg/kg/gün losartan oral olarak verildi. Deneyin 4. haftasının sonunda sıçanlar dekapite edilerek böbrek dokuları çıkartıldı. Rutin ışık mikroskobu takibi yapılarak dokular parafin bloklara gömüldü ve Periyodik Asit-Schiff (PAS) ile boyandı. Bulgular: Kontrol grubu glomerül ve tübül yapıları normal olarak izlendi. Diyabetik grupta bazı glomerüllerde Bowman mesafesinde daralma, mezangial matriks artışı ve tübüler dilatasyon saptandı. Ayrıca tübül epitellerinin fırçamsı kenarlarında ayrılma ve bozulmalar, tübül bazal membranlarında kalınlaşma, glukojenik vakuolizasyonu gösteren şeffaf görünümlü tübüller (Armanni-Ebstein lezyonları) ve tübül lümenine dökülmeler gözlendi. Çalışmada DM+ Enalapril grubu ile DM+ Losartan grubu birbirlerine benzer histolojiye sahip olup bu gruplarda glomerüllerde Bowman mesafesinde daralma ve mezangial matriks artışı izlendi. Tübüler dilatasyonlar ve Armani-Ebstein lezyonları ise diyabetik gruba göre daha az belirgindi. Tübül epitellerinin fırçamsı kenarlarındaki ayrılma ve bozulmalar daha az belirgindi. Sonuç: STZ ile deneysel olarak diyabet oluşturulan sıçanların böbrek dokusunda enalapril ve losartanın diyabetik nefropatinin histolojik bulguları üzerine etkili olduğu belirlendi.

Keywords

Diabetes mellitus enalapril losartan böbrek

References

  • 1. Powers AC. Diabetes Mellitus. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, (eds). Harrison’s principles of Internal Medicine. 16th ed. McGraw Hill, 2005; 2152- 2180.
  • 2. Kahn CR, Weir GC, King GL, Jacobson AM, Moses AC, Smith RJ. Joslin’s Diabetes Mellitus. Fourteenth edition. Boston: Lippincott Williams and Wilkins, 2005; 331–338.
  • 3. Rahimi R, Nikfar S, Larijani B, Abdollahi M. A review on the role of antioxidants in the management of diabetes and its complications. Biomed Pharmacother 2005; 59: 365–373.
  • 4. Cooper ME. Interaction of metabolic and hemodynamic factors in mediating experimental diabetic nephropathy. Diabetologia 2001; 44: 1957–1972.
  • 5. Taniyama Y, Griendling KK. Reactive oxygen species in the vasculature: Molecular and cellular mechanisms. Hypertension 2003, 42: 1075–1081.
  • 6. Touyz RM. Reactive oxygen species and angiotensin II signaling in vascular cells implications in cardiovascular disease. Braz J Med Biol Res 2004; 37: 1263–1273.
  • 7. Touyz RM, Schiffrin EL. Ang II-stimulated superoxide production is mediated via phospholipase D in human vascular smooth muscle cells. Hypertension 1999; 34: 976–982.
  • 8. Onozato ML, Tojo A, Goto A, Fujita T, Wilcox CS. Oxidative stress and nitric oxide synthase in rat diabetic nephropathy: effects of ACEI and ARB. Kidney Int 2002; 61: 186 -194.
  • 9. Berry C, Anderson N, Kirk AJ, Dominiczak AF, McMurray JJ. Renin angiotensin system inhibition is associated with reduced free radical concentrations in arteries of patients with coronary heart disease. Heart 2001; 86: 217–220.
  • 10. Johansen JS, Harris AK, Rychly DJ and Ergul A. Oxidative stress and the use of antioxidants in diabetes: Linking basic science to clinical practice. Cardiovascular Diabetology 2005; 4: 5.
  • 11. Fan Q, Liao J, Kobayashi M, et al. Candesartan reduced advanced glycation end-products 56 accumulation and diminished nitro-oxidative stress in type 2 diabetic KK/Ta mice. Nephrol Dial Transplant 2004; 19: 3012–3020.
  • 12. Kumar V, Cotran RS, Robbins SL. Temel Patoloji, Prof. Dr. Uğur Çevikbaş (ed). s:511–517. 6. Baskı, Nobel Tıp Kitabevi, İstanbul, 2000.
  • 13. Ronco C, La Greca G. Vitamin E bonded membrane, a further step in dialysis optizimation. Contrib Nephrol 1999; 127: 1– 31.
  • 14. Sies H. Oxidants and antioxidants. Exp Physiol 1997; 82: 291- 295.
  • 15. Altan N, Dinçel AS, Koca C, Diabetes Mellitus ve Oksidatif Stres Türk Biyokimya Dergisi 2006; 31; 51–56.
  • 16. Tesfamariam B. Free radicals in diabetic endothelial dysfunction. Free Radic Biol Med 1994;16: 383–391.
  • 17. Komers R, Lindsley JN, Oyama TT, Allison KM, Anderson S. Role of neuronal nitric oxide synthase (NOS1) in the pathogenesis of renal hemodynamic changes in diabetes. Am J Physiol Renal Physiol 2000; 279: 573–583.
  • 18. Esposito C, Liu ZH, Striker GE, et al. Inhibition of diabetic nephropathy by a GH antagonist: A molecular analysis. Kidney Int 1996; 50: 506–514.
  • 19. Lundbaek K, Christensen NJ, Jensen VA, et al. Diabetes, diabetic angiopathy, and growth hormone. Lancet 1970; 2: 131–133.
  • 20. Osterby R, Asplund J, Bangstad HJ, et al. Neovascularization at the vascular pole region in diabetic glomerulopathy. Nephrol Dial Transplant 1999; 14: 348–352.
  • 21. Cortes P, Dumler F, Goldman J, Levin NW. Relationship between renal function and metabolic alterations in early streptozocin-induced diabetes in rats. Diabetes 1987; 36: 80– 87.
  • 22. Sanai T, Sobka T, Johnson T, et al. Expression of cytoskeletal proteins during the course of experimental diabetic nephropathy. Diabetologia 2000; 43: 91–100.
  • 23. Tucker BJ, Collins RC, Ziegler MG, Blantz RC. Disassociation between glomerular hyperfiltration and extracellular volume in diabetic rats. Kidney Int 1991; 39: 1176–1183.
  • 24. New JP, Canavan JP, Flyvbjerg A, Hamon G, Bilous RW, Marshall SM. Renal enlargement and insulin-like growth factor–1 accumulation in the Wistar rat model of experimental diabetes is not prevented by angiotensin converting enzyme inhibition. Diabetologia 1996; 39: 166–171.
  • 25. Büyükdevrim AS, Büyükbeşe MA, Davutoğlu M. Diabetik nefropati. Klinik moleküler patogenez klasik ve moleküler tedavi. İstanbul: Turgut yayıncılık, 2005; 432–529, 136–342.
  • 26. De Cavanagh EMV, Inserra F, Toblli J, Stella I, Fraga C.G and Ferder L. Enalapril Attenuates Oxidative Stress in Diabetic Rats. Hypertension 2001; 38: 1130–1136.
  • 27. Dönmez S. Deneysel Diabetik Nefropatide İrbesartan ve Antioksidan Tedavilerin Karşılaştırılması, Uzmanlık Tezi 2008; 46–58.
There are 27 citations in total.

Details

Primary Language Turkish
Journal Section Articles
Authors

Mehmet Murat Doğan This is me

Emir Dönder This is me

Tuncay Kuloğlu This is me

Dürrin Özlem Dabak This is me

Publication Date April 1, 2011
Published in Issue Year 2011 Volume: 16 Issue: 2

Cite

APA Doğan, M. M., Dönder, E., Kuloğlu, T., Dabak, D. Ö. (2011). Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi. Fırat Tıp Dergisi, 16(2), 46-50.
AMA Doğan MM, Dönder E, Kuloğlu T, Dabak DÖ. Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi. Fırat Tıp Dergisi. April 2011;16(2):46-50.
Chicago Doğan, Mehmet Murat, Emir Dönder, Tuncay Kuloğlu, and Dürrin Özlem Dabak. “Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril Ve Losartan’ın Etkilerinin İncelenmesi”. Fırat Tıp Dergisi 16, no. 2 (April 2011): 46-50.
EndNote Doğan MM, Dönder E, Kuloğlu T, Dabak DÖ (April 1, 2011) Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi. Fırat Tıp Dergisi 16 2 46–50.
IEEE M. M. Doğan, E. Dönder, T. Kuloğlu, and D. Ö. Dabak, “Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi”, Fırat Tıp Dergisi, vol. 16, no. 2, pp. 46–50, 2011.
ISNAD Doğan, Mehmet Murat et al. “Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril Ve Losartan’ın Etkilerinin İncelenmesi”. Fırat Tıp Dergisi 16/2 (April 2011), 46-50.
JAMA Doğan MM, Dönder E, Kuloğlu T, Dabak DÖ. Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi. Fırat Tıp Dergisi. 2011;16:46–50.
MLA Doğan, Mehmet Murat et al. “Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril Ve Losartan’ın Etkilerinin İncelenmesi”. Fırat Tıp Dergisi, vol. 16, no. 2, 2011, pp. 46-50.
Vancouver Doğan MM, Dönder E, Kuloğlu T, Dabak DÖ. Deneysel Diyabetin Sıçan Böbrek Dokusunda Meydana Getirdiği Değişiklikler Üzerine Enalapril ve Losartan’ın Etkilerinin İncelenmesi. Fırat Tıp Dergisi. 2011;16(2):46-50.