Antioxidant treatments improve diabetes induced endothelium-dependent vascular dysfunction


Zeydanli E., TURAN B.

Erciyes Tip Dergisi, cilt.31, sa.3, ss.193-200, 2009 (ESCI) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 31 Sayı: 3
  • Basım Tarihi: 2009
  • Dergi Adı: Erciyes Tip Dergisi
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.193-200
  • Anahtar Kelimeler: Selenium, Long chain (n-3) fatty acid, Aorta, Relaxation, Muscarinic Receptors, cyclic AMP
  • Lokman Hekim Üniversitesi Adresli: Hayır

Özet

Purpose: Diabetes is an important cardiovascular risk factor and impaired endothelium-dependent relaxation has been demonstrated in vascular beds of different models of diabetes. Hyperglycemia causes important changes in cells due to increased production of reactive oxygen species (ROS) and different types of receptor-mediated vasorelaxation can change during diabetes. Material and Methods: In our previous studies we have shown that antioxidant treatment improved diabetes-induced alterations in heart function. Therefore, in this study we aimed to evaluate the effect of treatment with either sodium selenate (0.3 mg/kg/day, intragastrically) or a long chain (n-3) polyunsaturated fatty acid enriched with vitamin E (omega-3E; 50 mg/kg/day, intragastrically) on mechanical function of streptozotocin (STZ)-induced diabetic rat aortas for 4-week. Results: Both types of treatments improved the impaired relaxation responses to acetylcholine (ACh; 10-9.10-4 M) of endothelium-intact (pre-contracted with phenylephrine; 10-6 M) aortas. Furthermore, these treatments prevented diabetes-induced decreased level of cAMP production with ACh stimulation. Conclusion: Taken together, our data demonstrate that these beneficial effects of both sodium selenate and omega-3E on the mechanical properties of the diabetic aortas appear, in part, to be related to inhibition of ROS production and regulation of cell antioxidant state arised in diabetic vascular dysfunction.