Panax notoginseng saponins protect kidney from diabetes by up-regulating silent information regulator 1 and activating antioxidant proteins in rats

Chin J Integr Med. 2016 Dec;22(12):910-917. doi: 10.1007/s11655-015-2446-1. Epub 2015 Dec 28.


Objective: To explore the mechanism of the protective effects of Panax notoginseng saponins (PNS) on kidney in diabetic rats.

Methods: Diabetic rat model was obtained by intravenous injection of alloxan, and the rats were divided into model, PNS-100 mg/(kg day) and PNS-200 mg/(kg day) groups, 10 each. Another 10 rats injected with saline were served as control. Periodic acid-Schiff staining and immunological histological chemistry were used to observe histomorphology and tissue expression of bone morphogenetic protein-7 (BMP-7). Silent information regulator 1 (SIRT1) was silenced in rat mesangial cells by RNA interference. The mRNA expressions of SIRT-1, monocyte chemoattractant protein-1 (MCP-1), transforming growth factor β1 (TGF-β1) and plasminogen activator inhibitor-1 (PAI-1) were analyzed by reverse transcription polymerase chain reaction. The protein expressions of SIRT1 and the acetylation of nuclear factor κB (NF-κB) P65 were determined by western blotting. The concentration of MCP-1, TGF-β1 and malondialdehyde (MDA) in culture supernatant were detected by enzyme-linked immuno sorbent assay. The activity of superoxide dismutase (SOD) was detected by the classical method of nitrogen and blue four.

Results: In diabetic model rats, PNS could not only reduce blood glucose and lipid (P<0.01), but also increase protein level of BMP-7 and inhibit PAI-1 expression for suppressing fibrosis of the kidney. In rat mesangial cells, PNS could up-regulate the expression of SIRT1 (P<0.01) and in turn suppress the transcription of TGF-β1 (P<0.05) and MCP-1 (P<0.05). PNS could also reverse the increased acetylation of NF-κB p65 by high glucose. In addition, redox regulation factor MDA was down-regulated (P<0.05) and SOD was up-regulated (P<0.01), which were both induced by SIRT1 up-regulation.

Conclusions: PNS could protect kidney from diabetes with the possible mechanism of up-regulating SIRT1, therefore inhibiting inflammation through decreasing the induction of inflammatory cytokines and TGF-β1, as well as activating antioxidant proteins.

Keywords: Chinese medicine; Panax notoginseng saponins; diabetic nephropathy; inflammation; nuclear factor κB; silent information regulator 1.

MeSH terms

  • Acetylation / drug effects
  • Animals
  • Antioxidants / metabolism*
  • Blood Glucose / metabolism
  • Bone Morphogenetic Protein 7 / metabolism
  • Chemokine CCL2 / metabolism
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / drug therapy*
  • Diabetes Mellitus, Experimental / genetics
  • Diabetes Mellitus, Experimental / physiopathology
  • Gene Knockdown Techniques
  • Immunohistochemistry
  • Kidney / drug effects
  • Kidney / pathology*
  • Kidney Function Tests
  • Lipids / blood
  • Male
  • Malondialdehyde / metabolism
  • Mesangial Cells / drug effects
  • Mesangial Cells / metabolism
  • Oxidative Stress / drug effects
  • Panax notoginseng / chemistry*
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / metabolism
  • Protective Agents / pharmacology
  • Protective Agents / therapeutic use*
  • Rats, Sprague-Dawley
  • Saponins / pharmacology
  • Saponins / therapeutic use*
  • Sirtuin 1 / genetics*
  • Superoxide Dismutase / metabolism
  • Transcription Factor RelA / metabolism
  • Transcription, Genetic / drug effects
  • Transforming Growth Factor beta1 / metabolism
  • Up-Regulation / drug effects*


  • Antioxidants
  • Blood Glucose
  • Bone Morphogenetic Protein 7
  • Chemokine CCL2
  • Lipids
  • Plasminogen Activator Inhibitor 1
  • Protective Agents
  • Saponins
  • Transcription Factor RelA
  • Transforming Growth Factor beta1
  • Malondialdehyde
  • Superoxide Dismutase
  • Sirtuin 1