Conclusion: The results of this study indicate that diabetes causes up-regulation of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS), which may be involved in the pathogenesis of cochlea functional loss.
Objective: To investigate the underlying mechanisms that may be responsible for diabetic microangiopathy in the inner ear, we studied the expression of VEGF, iNOS, and eNOS in the streptozotocin (STZ)-induced diabetic rat cochlea.
Materials and methods: The immunofluorescence studies were performed by using FITC-labelled specific antibodies to VEGF, iNOS, and eNOS on paraffin sections of the cochlea. The expression levels of VEGF, iNOS, and eNOS were quantified by means of Western blot analysis of cochlea protein extracts. Evans blue (EB) was used to investigate blood-labyrinth barrier (BLB) permeability in the cochlea.
Results: Increased cochlear expression of VEGF, iNOS, and eNOS was detected in the diabetic rat. Furthermore, increased permeability of BLB was evidenced by increased cochlear EB extravasation in the diabetic rat.