Upregulation of osteopontin expression in renal cortex of streptozotocin-induced diabetic rats is mediated by bradykinin.

摘要: The model of streptozotocin (STZ)-induced diabetes in Wistar rats was used to study the expression osteopontin during development diabetic nephropathy. Diabetes confirmed by serum glucose levels exceeding 16 mmol/l experimental period 12 weeks. During this time, nephropathy developed, as characterized a reduced glomerular filtration rate (2.7 +/- 0.3 ml/min controls vs. 1.7 0.1 rats) and proteinuria (8.3 mg/24 h 22.0 4 rats). Northern blot analysis revealed time-dependent upregulation renal cortical reaching 138 6% control after 2 weeks 290 30% (mean SE, n = 6-9) By immunostaining, increased could be located tubular epithelium cortex. Chronic treatment animals with ramipril (3 mg/kg) 12-week led further increase mRNA animals, amounting 570 73% 6) controls. Increased were not associated accumulation monocyte/macrophages that identified cell type specific monoclonal antibody ED-1. ramipril-pretreated abolished application bradykinin B2-receptor antagonist, icatibant (0.5 mg/kg). In addition, rats, which did receive any STZ injection, well given for final period. These data suggest strong B2-receptor-mediated occurs pathogenesis rats.