The impact of vitamin E supplementation on urinary bladder contractility in streptozotocin-induced diabetic rats

Abstract

Background: To determine whether vitamin E protects streptozotocin-induced diabetic rats from diabetic urinary bladder dysfunction and discover its possible mechanism. Materials and Methods: A total of 40 rats were randomly divided into four groups: a control group (A), a diabetic group (B), a group given vitamin Eonly (C), and a diabetic group given vitamin E therapy for 8 weeks (D). Diabetes was induced in the rats by 65 mg/kg streptozosin (STZ) via an intraperitoneal (i.p.) injection. Vitamin E was given in a dose of 50 mg/kg/day i.p. Under urethane anaesthesia (1.2 g/kg) subcutaneously and decapitation, contractile responses to carbachol of detrusor strips in all groups were studied in vitro. The levels of nitrite, nitrate, malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were detected in bladder tissues homogenates. Apoptosis studies were performed by detection of the levels of caspase 3 and cell death detection. Results: The bladder weights were significantly increased (p<0.001) in diabetic groups compared to the other studied groups. Contractile responses to carbachol increased in the diabetic group more than in the other groups (p<0.001). Vitamin E improved the contractile responses of group D and improved them but still significantly higher than those of control group (p < 0.05). Vitamin E treatment decreased the tissue MDA, nitrite, nitrate and GSH levels of group D which were significantly higher in group B than A and C groups (p<0.001). All enzyme activities of group B were significantly lower than those of the other groups, although they increased significantly in group D but still lower than those of A and C groups. However, no significant differences were detected between the levels of GPx and SOD of group D and those of A and C groups. Conclusions: These data suggest that vitamin E supplementation may be beneficial in delaying the progression of diabetic dysfunction in experimental animal model.