Objectives: 

To determine whether vitamin E has protective effects or not on streptozotocin-induced diabetic rats in diabetic urinary bladder dysfunction and discover its possible mechanism.

Materials: 

A total of 40 rats were randomly divided into four groups: a control group (A), a diabetic group (B), a group given vitamin E only (C), and a diabetic group given vitamin E therapy for 8 weeks(D). Diabetes was induced in the rats by 65 mg/kg STZ via an intraperitoneal (i.p.) injection. Vitamin E was given 50 mg/kg/day. Under urethane anaesthesia (1.2 g/kg) subcutaneously,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 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 increased in the diabetic group to carbachol than in the other groups (p<0.001). Vitamin E improved the contractile responses and improved them nearly to that of the control group but still significantly higher (p< 0.05). Vitamin E treatment decreased the tissue MDA,nitrite ,nitrate and GSH levels of group D which were in group B significantly higher than those of group A and C groups (p<0.001). All enzymes 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 suggests that vitamin E supplementation may be beneficial in delaying the progression of diabetic cystopathy in experimental animal model.