Finally it will be unfair if I ignore the ever uncontestable companionship of kopparberg, I am indeed indebted to the manufacturers. Abstract The potential role of a carboxypeptidase B2 inhibitor in renal fibrosis Diabetic nephropathy (DN) is a fibrotic disease from injury which is characterized by extracellular matrix (ECM) build-up. Thus, DN leads to disruption of renal architecture and loss of renal function. We hypothesized that renal fibrosis can be improved by increasing plasmin activity through inhibition of carboxypeptidase B2 (CPB2) activity using UK-396082- a selective CPB2 inhibitor. An in vivo rat of DN was used. Unilateral nephrectomy and induction of type 1 diabetes with 80mg/kg streptozotocin injection. Blood glucose was maintained between 20-25 mM for 8 months with linplants. The rats were divided into 3 groups. Group 1 (diseased) fed on normal chow. Group 3 (treatment) fed on normal chow for four months after which it was changed to chow mixed with 0.3g/kg of UK-396082 for the final four months. Group 2 (prophylaxis) fed on chow mixed with a 0.3g/kg of for 8 month. In an in study CPB2, plasmin, tissue–type (tPA) and urokinase-type (uPA) plasminogen activators were assayed in the presence and absence of UK-396082 in rat kidney fibroblast-like and mesangial cells cultured on plastic and fibrin gel. Our results confirmed DN in this rat model. Prophylactic
Finally it will be unfair if I ignore the ever uncontestable companionship of kopparberg, I am indeed indebted to the manufacturers. Abstract The potential role of a carboxypeptidase B2 inhibitor in renal fibrosis Diabetic nephropathy (DN) is a fibrotic disease from injury which is characterized by extracellular matrix (ECM) build-up. Thus, DN leads to disruption of renal architecture and loss of renal function. We hypothesized that renal fibrosis can be improved by increasing plasmin activity through inhibition of carboxypeptidase B2 (CPB2) activity using UK-396082- a selective CPB2 inhibitor. An in vivo rat of DN was used. Unilateral nephrectomy and induction of type 1 diabetes with 80mg/kg streptozotocin injection. Blood glucose was maintained between 20-25 mM for 8 months with linplants. The rats were divided into 3 groups. Group 1 (diseased) fed on normal chow. Group 3 (treatment) fed on normal chow for four months after which it was changed to chow mixed with 0.3g/kg of UK-396082 for the final four months. Group 2 (prophylaxis) fed on chow mixed with a 0.3g/kg of for 8 month. In an in study CPB2, plasmin, tissue–type (tPA) and urokinase-type (uPA) plasminogen activators were assayed in the presence and absence of UK-396082 in rat kidney fibroblast-like and mesangial cells cultured on plastic and fibrin gel. Our results confirmed DN in this rat model. Prophylactic