Peroxisome proliferator-activated receptor γ prevents the production of NOD-like receptor family, pyrin domain containing 3 inflammasome and interleukin 1β in HK-2 renal tubular epithelial cells stimulated by monosodium urate crystals

Abstract

Recent evidence showed that peroxisome proliferator‑activated receptor γ (PPARγ) ameliorates a variety of inflammatory conditions. The present study aimed to investigate the role of PPARγ in regulating NOD-like receptor family, pyrin domain containing 3 (NALP3) inflammasome and interleukin (IL)‑1β levels during monosodium urate (MSU) crystal‑induced inflammation. HK‑2 cells were incubated with or without 200 µg/ml MSU crystals, and mRNA and protein levels of PPARγ were determined using reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively. To verify the role of PPARγ, HK‑2 cells were pre‑treated with PPARγ agonist pioglitazone, and the levels of NALP3 inflammasome and IL‑1β were detected by western blot analysis and ELISA. The results showed that MSU crystals increased PPARγ expression in HK‑2 cells at 24 h, while the expression decreased to normal levels at 48 h. It was also demonstrated that although the PPARγ agonist pioglitazone did not alter the mRNA and protein levels of PPARγ, it significantly reduced the MSU crystal‑induced production of NALP3 inflammasome and IL‑1β in HK‑2 cells, possibly by increasing the level of PPARγ activity. In conclusion, the results of the present study indicated that PPARγ prevented NALP3 inflammasome formation and IL‑1β production in HK‑2 cells stimulated by MSU crystals, which indicated that PPARγ may represent a novel target for the treatment of hyperuricemic nephropathy.