Supplementary material-blots.pdf (213.44 kB)
Download file

Supplementary Material for: Pterostilbene, a resveratrol derivative, improves ectopic lipid deposition in the kidneys of mice induced by a high-fat diet

Download (213.44 kB)
dataset
posted on 17.06.2022, 08:39 authored by Gu W., Yang L., Wang X., Geng J., Li X., Zheng K., Guan Y., Hou X., Wang C., Song G.
Background: Diabetic kidney disease is a major cause of global end-stage renal diseases. Ectopic lipid deposition in the renal tissues of diabetic kidney disease is one major factor leading to renal fibrosis and chronic kidney disease. Pterostilbene has been reported to display lipid-lowing activity and participate in many kidney diseases. However, the influence of pterostilbene on the ectopic lipid deposition is unclear. We intend to explore the influence of pterostilbene on the ectopic lipid deposition in the kidney of mice induced by high fat. Methods: A high-fat diet-induced diabetic mouse model was established to detect the alleviative effect of pterostilbene on the ectopic lipid deposition in the kidney of diabetic mice. Biochemical analysis was performed to examine the level of urine albumin, urine creatinine, serum creatinine and blood urea nitrogen in mice after pterostilbene treatment. Histological analysis was conducted to detect the degree of renal injury and fibrosis. Oil red O staining and immunohistochemical staining were carried out to evaluate lipid droplets and the expression of adipose differentiation-related protein (ADRP) in renal tissues of the mice treated by pterostilbene. The protein levels were assessed by western blotting. Results: Pterostilbene inhibits the expression of the TGF-β1 and p-smad3 and suppresses the protein levels of SREBP-1 and FAS, and ultimately reduces the ectopic lipid deposition and alleviates the renal tubular damage and renal fibrosis in the kidneys of diabetic mice induced by high fat, and improved kidney function. Conclusion: Pterostilbene alleviates renal fibrosis and ectopic lipid deposition in the kidneys of diabetic mice induced by high fat diet by inhibiting the TGF-β1/smad3 signaling.

History