Improvement of Endothelium-Dependent Relaxation in Aorta of Rat Models Type 1 and 2 Diabetes by Hespiridin

authors:

avatar A Kouhpayeh 1 , avatar H Mirkhani 2 , * , avatar Ali Akbar Nekooeian 3

Department of Pharmacology, Medical School, Iran
Medicinal & Natural Products Chemistry Research Centre, Iran
Cardiovascular Pharmacology Research Center, Department of Pharmacology, Shiraz University of Medical Sciences Shiraz, Iran

how to cite: Kouhpayeh A , Mirkhani H , Nekooeian A A . Improvement of Endothelium-Dependent Relaxation in Aorta of Rat Models Type 1 and 2 Diabetes by Hespiridin. Int Cardiovasc Res J. 2007;1(4):e69298. 

Abstract

Background: Vascular disease is the principal cause of morbidity and mortality in patients with diabetes. A
considerable body of evidence implicates oxidative stress as an important pathogenic factor of diabetic vasculopathies.
In the present study, the effect of hesperidin, a flavanone glycoside with antioxidant activity, is studied
in endothelium-dependent relaxation of the rat aorta in experimental diabetes mellitus type 1 (DM1) and type 2
(DM2).
Patients and Methods: Single dose intraperitoneal injection of streptozocin (60mg/kg) and subcutaneous daily
injection of dexamethasone (10μg/kg for one month) were used to induce DM1 and DM2, respectively. Hesperidin
(500mg/kg) was administered orally for two months in DM1 and one month in DM2. The effect of acetylcholine
(Ach) on phenyl ephrine (PE) induced. PE contracted aorta was then studied and the EC50 and maximal
relaxant effect of Ach were calculated and compared in the two groups.
Results: In the experimental DM1, hesperidin restored endothelium-dependent relaxation near to those of normal
animals. Its effect on experimental DM2 consisted of a significant reduction of EC50 value of Ach compared
to those of diabetic animals. It also showed a great but non-significant effect (P=0.07) on Ach-induced maximum
relaxation compared to DM2 untreated animals.
Conclusion: These results show that hesperidin can improve vascular endothelial dysfunction in experimental
diabetes mellitus.

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References

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