Journals / Akdeniz Tıp Dergisi / 2020 / Cilt: 6 - Sayı: 2

The Effects of Losartan on Lipid Peroxidation and the Antioxidant System in the Bone Tissue of Diabetic Rats

Diyabetik Sıçanlarda Kemik Dokusunda Lipid Peroksidasyonu ve Antioksidan Sistem Üzerine Losartan’ın Etkileri

Pages
219–225
Publication Date
2022-10-11
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)

Conclusion: These findings indicate that losartan can prevent bone loss and improve the quality of diabetic rat femurs, most probably to reduction of reactive oxygen species and/or modulation of antioxidant enzymes

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Diabetes leads to bone disorders such as osteopenia and osteoporosis that can increase the fracture risk and free radicals have been suggested to play significant role in the bone resorption associated with diabetes.
📊
Key Findings & Data:Diabetes was induced by single injection of streptozotocin 50 mg/kg .
💡
Conclusion & Impact:Conclusion: These findings indicate that losartan can prevent bone loss and improve the quality of diabetic rat femurs, most probably to reduction of reactive oxygen species and/or modulation of antioxidant enzymes
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Diyabet · Losartan · Oksidatif stres

Abstract

Objective: Diabetes leads to bone disorders such as osteopenia and osteoporosis that can increase the fracture risk and free radicals have been suggested to play significant role in the bone resorption associated with diabetes. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers may reduce bone loss and fracture risk in diabetic patients. This study was therefore designed to investigate the effects of losartan on bone quality and the antioxidant defense system in diabetic rat femurs.Material and Methods: The rats were divided into four groups: Control C , diabetes D , losartan-treated diabetes D-LOS and losartan-treated control C-LOS . Diabetes was induced by single injection of streptozotocin 50 mg/kg . The treated rats received 5 mg/kg/day of losartan for 8 weeks. Superoxide dismutase SOD , catalase CAT and glutathione peroxidase GPx activities and 2-thiobarbituric acid reactive substances TBARS levels were analyzed in bone tissue samples.Results: Diabetes revealed a highly significant increase in the TBARS values of rat bones and losartan administration significantly lowered the TBARS levels. SOD activity was decreased in group D but no change in CAT activity was observed and losartan treatment did not affect SOD activity. Diabetes resulted in a marked decrease in GPx that was increased significantly by losartan. Conclusion: These findings indicate that losartan can prevent bone loss and improve the quality of diabetic rat femurs, most probably to reduction of reactive oxygen species and/or modulation of antioxidant enzymes

Özet

Amaç: Diyabet, kırık riskini artırabilecek osteopeni ve osteoporoz gibi kemik hastalıklarına yol açarken, serbest radikallerin diyabetle ilişkili kemik rezorpsiyonunda önemli rol oynadığı öne sürülmüştür. Anjiyotensin-dönüştürücü enzim inhibitörleri ve anjiyotensin reseptör blokörlerinin diyabetik hastalarda kemik kaybını ve kırılma riskini azaltabilmesi muhtemeldir. Bu nedenle çalışmamız, diyabetik sıçan femurlarında losartanın oksidatif stres ve antioksidan savunma sistemi üzerindeki etkilerini araştırmak ve böylece kemik kalitesindeki bozulmanın olası mekanizmasını açıklamak için tasarlanmıştır.Gereç ve Yöntemler: Sıçanlar dört gruba ayrılmıştır: Kontrol K , diyabet D , losartanla tedavi edilen diyabet D-LOS ve losartanla tedavi edilen kontrol K-LOS . Diyabet, tek doz streptozotosin 50 mg/kg enjeksiyonu ile indüklenmiştir. Diyabetli sıçanlara 8 hafta boyunca 5 mg/kg/gün losartan uygulanmıştır. Kemik dokularında, 2-tiobarbiturik asit reaktif ürünlerinin düzeyi TBARS , süperoksit dismutaz SOD , katalaz KAT ve glutatyon peroksidaz GPx aktiviteleri incelenmiştir.Bulgular: Diyabet uygulaması ile kemik dokuda anlamlı düzeyde artan TBARS değerleri losartan uygulaması ile düşmüştür. Diğer yandan, D grubunda SOD aktivitesi azalırken KAT aktivitesinde bir değişiklik gözlenmemiştir ve losartan tedavisi SOD aktivitesi üzerinde etkili olmamıştır. Diyabet ile birlikte anlamlı düzeyde düşen GPx aktivitesi losartan tedavisi ile normal seviyelerine dönmüştür.Sonuç: Bu bulgular, losartan tedavisinin diyabetik sıçan femurunda oksidatif stresin indüklediği kemik kalitesindeki düşüşü antioksidan enzimlerin modülasyonunu sağlayarak düzeltebileceğini göstermektedir

🔖

Cite This Article

ÖZDEMİR, S., OĞUZ, N., ERBOĞA, N. Ö., DÖNMEZ, B. Ö. (2022). The Effects of Losartan on Lipid Peroxidation and the Antioxidant System in the Bone Tissue of Diabetic Rats. Akdeniz Tıp Dergisi, Cilt: 6 - Sayı: 2, 219–225. https://ajindex.com/articles/434321

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Beam HA, Parsons JR, Lin SS. The effects of blood glucose control upon fracture healing in the BB Wistar rat with diabetes mellitus. J Orthop Res 2002; 20(6):1210-6.
  2. Lieberman D, Fried V, Castel H, Weitzmann S, Lowenthal MN, Galinsky D. Factors related to successful rehabilitation after hip fracture: A case-control study. Disabil Rehabil 1996; 18(5):224-30. Schwartz AV. Diabetes Mellitus: Does it affect bone? Calcif Tissue Int 2003; 73(6):515-9. Özdemir S. Anjiyotensin II Reseptörünün Deneysel Diyabetik Sıçan Kalbi Elektriksel Aktivitesindeki Rolü. Doktora Tezi. Ankara: Ankara Üniversitesi, 2004.
  3. Inzerillo AM, Epstein S. Osteoporosis and diabetes mellitus. Rev Endocr Metab Disord 2004; 5(3):261-8.
  4. Keegan TH, Kelsey JL, Sidney S, Quesenberry CP Jr. Foot problems as risk factors of fractures. Am J Epidemiol 2002; 155(10):926-31.
  5. Nicodemus KK, Folsom AR. Type 1 and type 2 diabetes and incident hip fractures in postmenopausal women. Diabetes Care 2001; 24(7):1192-7.
  6. Schwartz AV, Sellmeyer DE, Ensrud KE, Cauley JA, Tabor HK, Schreiner PJ, Jamal SA, Black DM, Cummings SR. Older women with diabetes have an increased risk of fracture: A prospective study. J Clin Endocrinol Metab 2001; 86(1):32-8.
  7. Reddy GK, Stehno-Bittel L, Hamade S, Enwemeka CS. The biomechanical integrity of bone in experimental diabetes. Diabetes Res Clin Pract 2001; 54(1):1-8.
  8. Hamada Y, Kitazawa S, Kitazawa R, Fujii H, Kasuga M, Fukagawa M. Histomorphometric analysis of diabetic osteopenia in streptozotocin-induced diabetic mice: A possible role of oxidative stress. Bone 2007; 40(5):1408-14.
  9. Mody N, Parhami F, Sarafian TA, Demer LL. Oxidative stress modulates osteoblastic differentiation of vascular and bone cells. Free Radic Biol Med 2001; 31(4):509-19.
  10. Bai XC, Lu D, Bai J, Zheng H, Ke ZY, Li XM, Luo SQ. Oxidative stress inhibits osteoblastic differentiation of bone cells by ERK and NF-kappaB. Biochem Biophys Res Commun 2004; 314(1):197-207.
  11. Chen RM, Wu GJ, Chang HC, Chen JT, Chen TF, Lin YL, Chen TL. 2,6-Diisopropylphenol protects osteoblasts from oxidative stress-induced apoptosis through suppression of caspase-3 activation. Ann N Y Acad Sci 2005; 1042:448-59.
  12. Fatokun AA, Stone TW, Smith RA. Hydrogen peroxide- induced oxidative stress in MC3T3-E1 cells: The effects of glutamate and protection by purines. Bone 2006; 39(3): 542-51.
  13. Dinh DT, Frauman AG, Johnston CI, Fabiani ME. Angiotensin receptors: Distribution, signalling and function. Clin Sci (Lond) 2001; 100(5): 481-92.
  14. Izu Y, Mizoguchi F