Document Type : Research Paper
Department of Cardiology, Faculty of Medicine, Shahed University, Tehran, Iran.
Neurophysiology Research Center, Shahed University, Tehran, Iran
Medical Students Research Committee, Shahed University, Tehran, Iran
Faculty of Medicine, Shahed University, Tehran, Iran
Medical Students Scientific Association, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
Department of Cellular and Molecular Biology, Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran
Objective: The current study aimed at evaluating the effect of flavonoid apigenin on contractile response and relaxation of aorta in streptozotocin (STZ)-induced diabetic rats.
Materials and Methods: Thirty-two rats were randomly divided into four groups of control, apigenin, diabetic (DM), and DM + apigenin. DM was induced in rats using intraperitoneal (i.p.) injection of STZ at 60 mg/kg. The two treatment groups received apigenin at a dose of 10 mg/kg i.p. every other day for four weeks. At the end of the study, the contractile responses of aorta to potassium chloride (KCL), phenylephrine (PE), and the relaxation response of the aorta to acetylcholine (ACh) were measured.
Results: Treatment with apigenin significantly reduced plasma glucose in diabetic rats in the 2nd and 4th weeks as compared to those of the DM group (P = 0.01). The DM+apigenin group had less contractile response as compared to that of the DM group, although the difference was not statistically significant (P >0.05). Treatment of diabetic rats with apigenin could significantly reduce the maximum contractile response as compared to that of the DM group (P = 0.05). The contractile response to ACh was significantly higher in the DM + apigenin group as compared to that of the DM group (P = 0.05).
Conclusion: The results of the current study indicated the hypoglycemic effects of apigenin in diabetic rats. In addition, it was observed that the administration of apigenin to diabetic and healthy rats could reduce contractile response of aorta to PE and increase the relaxation response to ACh.