Background: Diabetic nephropathy is one of the major causes leading to end-stage renal failure. There are conflicting reports about the impact of treatment with statins on the diabetic nephropathy through their anti-inflammatory effect. Local cytokine levels and activity are of great value for monitoring of pathological events in a target tissue. So, cytokines measurements in tissue or peripheral circulation have been an important part of the process of defining their role in health and disease. Cystatin-C is an alternative serum biomarker that has been proposed for estimating renal function that can replace or supplement serum creatinine.
Objective: Evaluation of the possible effect of atorvastatin treatment on the renal damage caused by type-1 diabetes mellitus in the terms of renal inflammatory cytokines and serum Cystatin-C.
Materials and Methods: Thirty two male albino rats were divided into four equal groups, Group A: non-diabetic rats (negative controls), Group B: type-1 diabetic rats (positive controls), Group C: non-diabetic rats received oral atorvastatin for 4 weeks, and Group D: type-1 diabetic rats received oral atorvastatin for 4 weeks. At the end of the designated period, animals were sacrificed, kidneys and blood samples were collected; IL-1β, IL-6, IL-10 and prostaglandin E2 were determined in kidney homogenate, while Cystatin-C, creatinine and urea were assayed in serum.
Results: IL-1β, IL-6, IL-10 and PGE2 in diabetic rat kidney significantly elevated above control. In addition, serum Cystatin-C significantly elevated in the diabetic rats. Treatment of diabetic rats with atorvastatin caused decreases in all determined cytokines as well as Cystatin-C to levels near control values.
Conclusion: Atorvastatin has the potential for protecting diabetes-induced renal injury in terms of decreasing renal inflammatory cytokines and serum Cystatin-C. However, the possible protective effect of atorvastatin should be supported by clinical studies.
Background: Diabetic nephropathy is one of the major causes leading to end-stage renal failure. There are conflicting reports about the impact of treatment with statins on the diabetic nephropathy through their anti-inflammatory effect. Local cytokine levels and activity are of great value for monitoring of pathological events in a target tissue. So, cytokines measurements in tissue or peripheral circulation have been an important part of the process of defining their role in health and disease. Cystatin-C is an alternative serum biomarker that has been proposed for estimating renal function that can replace or supplement serum creatinine.
Objective: Evaluation of the possible effect of atorvastatin treatment on the renal damage caused by type-1 diabetes mellitus in the terms of renal inflammatory cytokines and serum Cystatin-C.
Materials and Methods: Thirty two male albino rats were divided into four equal groups, Group A: non-diabetic rats (negative controls), Group B: type-1 diabetic rats (positive controls), Group C: non-diabetic rats received oral atorvastatin for 4 weeks, and Group D: type-1 diabetic rats received oral atorvastatin for 4 weeks. At the end of the designated period, animals were sacrificed, kidneys and blood samples were collected; IL-1β, IL-6, IL-10 and prostaglandin E2 were determined in kidney homogenate, while Cystatin-C, creatinine and urea were assayed in serum.
Results: IL-1β, IL-6, IL-10 and PGE2 in diabetic rat kidney significantly elevated above control. In addition, serum Cystatin-C significantly elevated in the diabetic rats. Treatment of diabetic rats with atorvastatin caused decreases in all determined cytokines as well as Cystatin-C to levels near control values.
Conclusion: Atorvastatin has the potential for protecting diabetes-induced renal injury in terms of decreasing renal inflammatory cytokines and serum Cystatin-C. However, the possible protective effect of atorvastatin should be supported by clinical studies.