Effect of curcumin on vascular endothelial growth factor expression in diabetic mice kidney induced by streptozotocin

Abstract

Objective: To localize and demonstrate the effect of curcumin on vascular endothelial growth factor in diabetic mice kidney induced by streptozotocin Material and Method: Diabetic mice were induced by streptozotocin (60 mg/kg BW). Male mice were divided into three groups, control mice, diabetic mice (DM) and diabetic mice treated with curcumin (DMC) (200 mg/ kg BW). At 4 and 8 weeks, animals were sacrificed and kidneys were processed by immunohistochemistry technique. Results: At the end of 4 and 8 week experiments, glomeruli were slightly enlarged and showed diffuse thickening of the glomerular capillary walls in diabetic mice. Administration with curcumin presented the better improvement and recovery of cells and tissues compared with diabetic mice. Immunohistochemical staining for vascular endothelial growth factor (VEGF) demonstrated that VEGF was mainly detected in the podocytes and renal tubules. There was an increase in VEGF expression in diabetic mice as compared to control. Treatment with curcumin significantly inhibited the expression of VEGF in the kidney tissue of diabetic mice in both 4 and 8 weeks. Comparing the diabetic mice between 4 and 8 week experiments, the expression of VEGF in the podocytes and renal tubules at 8 week were significantly stronger than at 4 week which represented time-dependent change. Nevertheless, the intensity of VEGF was not different in DMC mice when it was compared between 4 and 8 weeks. Conclusion: VEGF immunoreactivity of the podocytes and the renal tubules at 4 and 8 weeks in DM mice showed strong intensity more than in control mice. However, the intensity of VEGF in DMC mice was less when it was compared with DM mice. Moreover, VEGF was a key modulator of angiogenesis and a potent mitogen for endothelial cells. These results demonstrated the potential use of antiangiogenic curcumin as a novel therapeutic agent in diabetic mellitus and maintain normal structure of the kidney.