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Issue 5, 2017
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Polydatin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation by inhibiting NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway

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Abstract

This study was designed to investigate the effects of polydatin (PLD) on potassium oxonate-induced hyperuricemic rats. Hyperuricemic rats were treated with potassium oxonate (250 mg kg−1) intragastrically for 7 days, and polydatin (25, 50 mg kg−1) or allopurinol (5 mg kg−1) was administered to the rats 1 h after the potassium oxonate exposure. Polydatin administration decreased the levels of uric acid and creatinine in serum and urine, leading to inhibition of pro-inflammatory cytokine production in serum and kidney. Western blot analyses illustrated that polydatin down-regulated the translocation of NF-κB p65, the degradation of IκBα, and the protein levels of inflammasome components (NLRP3, ASC, and caspase-1), which led to reduced IL-1β secretion. Notably, polydatin treatment activated AMP kinase (AMPK) protein and increased SIRT1 expression. Taken together, polydatin might be a promising agent for gouty treatment to inhibit renal NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway.

Graphical abstract: Polydatin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation by inhibiting NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway

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Publication details

The article was received on 24 Oct 2016, accepted on 31 Mar 2017 and first published on 05 Apr 2017


Article type: Paper
DOI: 10.1039/C6FO01561A
Citation: Food Funct., 2017,8, 1785-1792
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    Polydatin attenuates potassium oxonate-induced hyperuricemia and kidney inflammation by inhibiting NF-κB/NLRP3 inflammasome activation via the AMPK/SIRT1 pathway

    L. Chen and Z. Lan, Food Funct., 2017, 8, 1785
    DOI: 10.1039/C6FO01561A

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