[ effect of hesperidin, on cardiac dysfunction of experimental type-I diabetic rats]

Flavonoids are polyphenolic compounds, which are considered as antioxidants due to their ability to scavenge free radicals and inhibit enzymes in oxygen-reduction pathways. Various studies have shown that these products reduce the cardiovascular disease mortalities. Heart failure is one of the main cause of mortality in diabetic patients. It is believed that diabetes has deleterious cardiomyopathic effects, which would lead to heart failure. Several evidences indicate that oxidative stress is an important factor in the pathogenesis of diabetic complications, including cardiomyopathy. The objective of the present study was to examine the effects of hesperidin on cardiac function parameters in experimental diabetes mellitus type 1 [DM1]. Diabetes mellitus was induced in rats by single intraperitoneal injections of streptozotocin [60mg/kg]. diabetic rats were given oral Hesperidin [500 mg/kg] for two months. Afterwards, the animals' hearts were used to study left ventricular systolic pressure [LVSP], rate of rise [+dP/dT] and rate of decrease [-dP/dT] of left ventricular pressure, using Langendorff isolated heart apparatus. Diabetes significantly reduced the LVSP, +dP/dT and -dP/dT compared to the control group p<0.05]. Hesperidin significantly improved all measured parameters in diabetic animals [p<0.05]. These results show that hesperidin can improve diabetic cardiomyopathy in experimental diabetes mellitus

Improvement of endothelium-dependent relaxation in aorta of rat models type 1 and 2 diabetes by hespiridin

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]. Single dose intraperitoneal injection of streptozocin [60mg/kg] and subcutaneous daily injection of dexamethasone [10mg/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. 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. These results show that hesperidin can improve vascular endothelial dysfunction in experimental diabetes mellitus