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

Authors: Xie, X  Peng, J  Huang, K  Huang, J  Shen, X  Liu, P  Huang, H 
Citation: Xie X, etal., Mol Cell Endocrinol. 2012 Oct 15;362(1-2):183-93. doi: 10.1016/j.mce.2012.06.008. Epub 2012 Jun 22.
Pubmed: (View Article at PubMed) PMID:22732364
DOI: Full-text: DOI:10.1016/j.mce.2012.06.008

A number of studies have recently demonstrated the involvement of nuclear factor-kappa B (NF-kappaB) 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-kappaB, 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-kappaB 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-kappaB nuclear translocation, reduced the DNA-binding activity of NF-kappaB, as well as decreased the protein expression of ICAM-1 and TGF-beta 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-kappaB 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.

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CRRD Object Information
CRRD ID: 7205438
Created: 2013-01-02
Species: All species
Last Modified: 2013-01-02
Status: ACTIVE



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