SavedAdd your journal

Journals / Ege Tıp Dergisi / 2013 / Cilt: 52 - Sayı: 1

Glucose injury in diabetic rats' ovaries and effect of NF-kappa B way

Diyabetik sıçan overlerindeki glikoz hasarı ve NF-kappa B yolunun etkisi

H. G. PALA
O. ERBAŞ
F OLTULU
E. E. PALA
H. AKTUĞ
A. YAVAŞOĞLU
Pages
32–36
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Therefore, NF-kappa B inhibitors continue to be promising in preventing diabetic related tissue injury.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: To investigate glucose toxicity for ovarian damage severity and the effect of these by NF-kappa B way in rat models.
📊
Key Findings & Data:The group characteristics were compared by one-way ANOVA and Mann Whitney U test. p values less than 0.05 were accepted as significant.
💡
Conclusion & Impact:Therefore, NF-kappa B inhibitors continue to be promising in preventing diabetic related tissue injury.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: To investigate glucose toxicity for ovarian damage severity and the effect of these by NF-kappa B way in rat models. Materials and Methods: An experimental diabetes mellitus model was created in seven rats. All seven rats, whose blood glucose levels were normal, were included in the control group. After eight weeks; bilateral oophorectomy was performed and the ovaries were researched histologically. The group characteristics were compared by one-way ANOVA and Mann Whitney U test. p values less than 0.05 were accepted as significant. Results: There was a significant increase of follicular degeneration, stromal degeneration, stromal fibrosis and NF-kappa B immune-expression in diabetic rats' ovary when compared to the control group of normal rats (p=0,0001). Conclusion: Our study shows that glucose toxicity occured severely in the ovaries and this injury originated in the NF-kappa B way in diabetes mellitus. Therefore, NF-kappa B inhibitors continue to be promising in preventing diabetic related tissue injury.

Özet

Amaç: Bu çalışmada, sıçan modellerinde glikoz toksisitesinin overdeki hasarlanma şiddeti ve bu hasarın NF-kappa B üzerinden etkilerinin olup olmadığının araştırılması amaçlandı. Gereç ve Yöntem: Yedi adet sıçanda deneysel olarak diyabetes mellitus modeli oluşturuldu. Yedi adet kan glikoz seviyesi normal olan sıçan kontrol grubu olarak alındı. Sekiz hafta sonra over dokuları çıkarılıp histolojik olarak incelendi. Grupların özellikleri, tek yönlü ANOVA ve Mann Whitney U testi ile karşılaştırıldı. p<0.05 değerleri anlamlı olarak kabul edildi. Bulgular: Diyabetik sıçanların over dokusunda, kontrol grubu normal sıçanlarla karşılaştırıldığında; foliküler dejenerasyon, stromal dejenerasyon, stromal fibrozis ve NF-kappa B immunoekspresyonunun anlamlı olarak arttığı tespit edildi (p=0,0001). Sonuç: Çalışmamız glikoz toksisitesinin overde şiddetli olarak gerçekleştiğini ve bu hasarın NF-kappa B üzerinden olduğunu göstermektedir. Bu nedenle NF-kappa B inhibitörleri diyabete bağlı gelişen doku hasarını önlenmesinde ümit verici olmaya devam etmektedir.

🔖

Cite This Article

PALA, H. G., ERBAŞ, O., OLTULU, F., PALA, E. E., AKTUĞ, H., YAVAŞOĞLU, A. (2013). Glucose injury in diabetic rats' ovaries and effect of NF-kappa B way. Ege Tıp Dergisi, Cilt: 52 - Sayı: 1, 32–36. https://ajindex.com/articles/214531

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res 2010;107(9):1058-70
  2. Brownlee M. The pathobiology of diabetic complications: An unifying mechanism. Diabetes 2005;54(6):1615-25
  3. Yan SF, Ramasamy R, Schmidt AM. Mechanisms of Disease: Advanced glycation end-products and their receptor in inflammation and diabetes complications. Nat Clin Pract Endocrinol Metab 2008;4(5):285-93
  4. Herold K, Moser B, Chen Y, et al. Receptor for advanced glycation end products (RAGE) in a dash to the rescue: Inflammatory signals gone awry in the primal response to stress. J Leukoc Biol 2007;82(2):204-12
  5. Goldin A, Beckman JA, Schmidt AM, Creager MA. Advanced glycation end products: Sparking the development of diabetic vascular injury. Circulation 2006;114(6):597-605
  6. Yao D, Taguchi T, Matsumura T, et al. High glucose increases angiopoietin-2 transcription in microvascular endothelial cells through methylglyoxal modification of mSin3A. J Biol Chem 2007;282(42):31038-45
  7. Kolm-Litty V, Sauer U, Nerlich A, Lehmann R, Schleicher ED. High glucose-induced transforming growth factor beta1 production is mediated by hexosamine pathway in porcine glomerular mesangial cells. J Clin Invest 1998;101(1):160-9
  8. Queisser MA, Yao D, Geisler S, et al. Hyperglycemia impairs proteasome function by methylglyoxal. 2010;59(3):670-8
  9. Schatteman GC, Hanlon HD, Jiao C, Dodds SG, Christy BA. Blood derived angioblasts accelerate blood-flow restoration in diabetic mice. J Clin Invest 2000;106(4):571-8
  10. Gallagher KA, Liu ZJ, Xiao M, et al. Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1 alpha. J Clin Invest 2007;117(5):1249-59
  11. Pitkanen OM, Martin JM, Hallman M, Akerblom HK, Sariola H, Andersson SM. Free radical activity during development of insulin dependent diabetes mellitus in the rat. Life Sci 1992;50(5):335-9
  12. Gillery P, Monboisse JC, Maquart FX, Borel JP. Glycation of proteins as a source of superoxide. Diabetes 1988;14(1):1114-20
  13. Dinçer Y, Akçay T, Alademir Z, İlkova H. Effect of oxidative stress on glutathione pathway in red blood cells from patients with insulin-dependent diabetes mellitus. Metabolism 2002;51(10):1360-2
  14. Eidland A, Sebekova K, Schinzel R. Advanced glycation end products and the progressive course of renal disease. Am J Kidney Dis 2001;38 (4):100-6
  15. Giardino I, Edelstein D, Brownlee M. Bcl-2 expression or antioxidants prevent hypergl