الفهرس | Only 14 pages are availabe for public view |
Abstract Many agents have been tried in the prevention of nephropathy. There is an unmet need for improved renoprotective treatment in patients with diabetic nephropathy. The mechanisms by which blockade of MR decreases proteinuria in diabetic nephropathy is still elusive. Hyperglycemia, independent of aldosterone levels, induces podocyte injury through MR-mediated ROS production. MR blockade inhibits hyperglycemia-induced podocyte injury, focusing on the involvement of ROS production, in diabetic rats and cultured podocytes. In the present study, induction of DM in experimental rats was done by STZ and confirmed by elevated blood glucose level more than 350 mg/dl. STZ selectively destroys the pancreatic β-cells, which causes the inhibition of synthesis and release of insulin leading to the onset of Diabetes Mellitus. STZ-induced diabetic rats are usually accompanied with other clinical features i.e. polyuria, polydipsia, polyphagia and weight loss that stimulate a similar condition as seen in the human beings. |