Polydatin ameliorates experimental diabetes-induced fibronectin through inhibiting the activation of NF-κB signaling pathway in rat glomerular mesangial cells.

A number of studies have recently demonstrated the involvement of nuclear factor-kappa B (NF-κB) activation and the subsequent coordinated inflammatory responses in the pathogenesis of diabetic nephropathy (DN). Polydatin has been shown to have the ability of anti-adhesive inflammation. However, the possible protective and beneficial effects of polydatin on DN via suppressing inflammatory damage and extracellular matrix (ECM) accumulation are not fully elucidated. We found that the polydatin could inhibit the induction and activity of NF-κB, and meanwhile ameliorating ECM accumulation in streptozotocin-diabetic rats. We aimed to investigate the effect of polydatin on fibronectin (FN) protein expression, and to elucidate its potential mechanism involving the NF-κB inflammatory signaling pathway in rat glomerular mesangial cells (GMCs) cultured under high glucose. The results revealed that polydatin significantly suppressed high glucose-induced FN production, inhibited NF-κB nuclear translocation, reduced the DNA-binding activity of NF-κB, as well as decreased the protein expression of ICAM-1 and TGF-β in GMCs. These findings suggested that polydatin significantly represses high glucose-induced FN expression in rat GMCs, which may be closely related to its inhibition of the NF-κB signaling pathway. Hence, we elucidated the potential mechanisms of the anti-inflammatory effects and ECM accumulation alleviation of polydatin in GMCs of DN in vitro.
AuthorsXi Xie, Jing Peng, Kaipeng Huang, Juan Huang, Xiaoyan Shen, Peiqing Liu, Heqing Huang
JournalMolecular and cellular endocrinology (Mol Cell Endocrinol) Vol. 362 Issue 1-2 Pg. 183-93 (Oct 15 2012) ISSN: 1872-8057 [Electronic] Ireland
PMID22732364 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • Anti-Inflammatory Agents
  • Drugs, Chinese Herbal
  • Fibronectins
  • Glucosides
  • I-kappa B Proteins
  • NF-kappa B
  • Stilbenes
  • Transforming Growth Factor beta
  • Intercellular Adhesion Molecule-1
  • NF-kappaB inhibitor alpha
  • polydatin
  • Active Transport, Cell Nucleus
  • Animals
  • Anti-Inflammatory Agents (pharmacology, therapeutic use)
  • Cell Nucleus (metabolism)
  • Cells, Cultured
  • Cytoprotection
  • Diabetes Mellitus, Experimental (drug therapy, metabolism)
  • Diabetic Nephropathies (drug therapy, metabolism)
  • Drugs, Chinese Herbal (pharmacology, therapeutic use)
  • Fibronectins (metabolism)
  • Gene Expression (drug effects)
  • Glucosides (pharmacology, therapeutic use)
  • I-kappa B Proteins (metabolism)
  • Intercellular Adhesion Molecule-1 (genetics, metabolism)
  • Kidney (drug effects, metabolism, pathology)
  • Male
  • Mesangial Cells (drug effects, metabolism)
  • NF-kappa B (antagonists & inhibitors, metabolism)
  • Organ Size (drug effects)
  • Protein Binding
  • Proteolysis
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction
  • Stilbenes (pharmacology, therapeutic use)
  • Transforming Growth Factor beta (genetics, metabolism)

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