Islet transplantation alleviates podocyte injury in diabetic nephropathy rats

Abstract

Objective To investigate the mechanism of islet transplantation lessening renal damage of diabetic nephropathy (DN) rat model. Method Rat DN model was established by intraperitoneal injection of a single-dose streptozotocin. The rats were divided into normal control group, DN group and islet transplant group. Islet transplantation was taken on the right renal capsule in transplantation group at 8th week after the modeling. At week 12 after the modeling, the urinary protein, urinary creatinine and blood glucose in each group were determined. The kidneys were collected, and transplant islet HE staining, immunofluorescence, kidney electron microscopy were done. Synaptopodin and transforming growth factor-β1 (TGFβ1) protein expression was observed in renal tissues of each group by immunohistochemical staining. Result The urine protein and urinary creatinine ratio in islet transplant group was significantly lower than in DN group (P 0.05) with the control group, but was significantly lower than in DN group (P<0.05). Islet cells by HE staining and immunofluorescence staining showed new blood vessels around the islets, and the insulin secretion was exuberant. Under an electron microscope, there was local fusion of podocyte foot processes, and segmental thickening of the basement membrane in DN group; in islet transplant group, the foot processes of podocytes were neat, basement membrane structure was clear and had no thickening. Synaptopodin protein expression was significantly decreased in the glomeruli of DN group and islet transplant group as compared with the control group (P<0.05), and that in islet transplant group was significantly enhanced (P<0.05) as compared with DN group. The expression of TGFβ1 in DN group and islet transplant group was significantly increased (P<0.05) as compared with control group, and that in DN group was significantly higher (P<0.05) than in islet transplant group. Conclusion Islet transplantation can inhibit TGFβ1 pathway, improve DN podocyte injury in rats, and alleviate or even reverse proteinuria. Key words: Diabetic nephropathy; Islet transplantation; Podocyte