作者: Wenjuan Liu , Yeping Yang , Yemei Liu , Xiaolan Lu , Shizhe Guo
DOI: 10.1016/J.KINT.2016.06.018
关键词:
摘要: The kallikrein-kinin system has been shown to be involved in the development of diabetic nephropathy, but specific mechanisms are not fully understood. Here, we determined renal-protective role exogenous pancreatic kallikrein mice and studied potential db/db type 2 streptozotocin-induced 1 mice. After onset diabetes, were treated with either (db/db+kallikrein, streptozotocin+kallikrein) or saline (db/db+saline, streptozotocin+saline) for 16 weeks, while another group of received the same treatment after albuminuria (streptozotocin'+kallikrein, streptozotocin'+saline). Db/m littermates wild used as non-diabetic controls. Pancreatic had no effects on body weight, blood glucose pressure, significantly reduced among all three groups. Pathological analysis showed that decreased the thickness glomerular basement membrane, protected against effacement foot process, loss of endothelial fenestrae, prevented loss podocytes Renal fibrosis, inflammation oxidative stress kallikrein-treated mice compared expression kininogen1, tissue kallikrein, kinin B1 B2 receptors increased compared saline-treated Thus, both ameliorated which may mediated by activating system.