| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2814791 | Gene | 2016 | 6 Pages |
•PR enhances anti-oxidation capacity in diabetic nephropathy (DN) mice.•PR reduces kidney tissue damage of DN mice.•PR shows the hypoglycemic and renal protective effects in DN mice.•PR attenuates SIRT1/FOXO1 pathway for renal protection.
In this study, we evaluated the effect of puerarin (PR) on diabetic nephropathy (DN) in streptozotocin (STZ)-induced diabetic mice. The fasting blood glucose (FBG), blood urea nitrogen (BUN) and serum creatinine (Scr), as well as 24-hour urine protein levels were effectively ameliorated in DN mice treated with PR (20, 40, 80 mg/kg/day). Furthermore, PR treatment markedly resulted in down-regulation of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and reactive oxygen species (ROS) in kidney. Interestingly, the activities of manganese superoxide dismutase (MnSOD) and catalase (CAT) were increased by PR. An improvement in kidney tissue damage could be observed after PR administration. Further ultrastructural investigation revealed a dramatically ameliorative effect of PR on mitochondrial damage. Meanwhile, the silent information regulator 1 (SIRT1), forkhead box protein O1 (FOXO1) and alpha subunit of peroxisome proliferators-activated receptor-gamma coactivator-1 (PGC-1α) expressions were significantly up-regulated at protein level by PR administration in renal cortex. However, the protein expression of nuclear-factor kappa B (NF-κB) was down-regulated in PR groups. Our present study demonstrates the hypoglycemic and renal protective effects of PR in DN mice, which support its anti-diabetic property. PR exerts its renal protection effect probably via the mechanism of attenuating SIRT1/FOXO1 pathway for renal protection.
