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10.1155/2016/9605890

http://scihub22266oqcxt.onion/10.1155/2016/9605890
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C4789040!4789040!27022389
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suck abstract from ncbi


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pmid27022389      PPAR+Res 2016 ; 2016 (ä): ä
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  • Differential Roles of Peroxisome Proliferator-Activated Receptor-? and Receptor-? on Renal Crystal Formation in Hyperoxaluric Rodents #MMPMID27022389
  • Taguchi K; Okada A; Hamamoto S; Unno R; Kobayashi T; Ando R; Tozawa K; Gao B; Kohri K; Yasui T
  • PPAR Res 2016[]; 2016 (ä): ä PMID27022389show ga
  • Peroxisome proliferator-activated receptors (PPARs) and related inflammatory and oxidative molecule expression were investigated in a hyperoxaluric rodent model to evaluate the in vivo efficacy of PPAR agonists in preventing renal crystal formation. PPAR expression was examined in a mouse hyperoxaluria kidney stone model induced by daily intra-abdominal glyoxylate injection. Therapeutic effects of the PPAR? agonist fenofibrate and PPAR? agonist pioglitazone were also assessed in a 1% ethylene glycol-induced rat model of hyperoxaluria. Crystal formation, inflammation, cell injury, apoptosis, and oxidative stress were compared to those of vehicle-treated controls. Quantitative reverse transcription-polymerase chain reaction revealed that PPAR? and PPAR? expression decrease and increase, respectively, during crystal formation in hyperoxaluric kidneys. In addition, PPAR? localized to the cytoplasm of both proximal and distal tubular cells, whereas PPAR? accumulated in the nucleus of proximal tubular cells. Furthermore, renal crystal formation was significantly less prevalent in pioglitazone-treated rats but higher in the fenofibrate-treated and fenofibrate/pioglitazone-cotreated groups compared to controls, thus indicating that pioglitazone, but not fenofibrate, markedly decreased cell inflammation, oxidative stress, and apoptosis. Collectively, the results demonstrated that PPAR? suppressed renal crystal formation via its antioxidative and anti-inflammatory effects; however, the renotoxicity of PPAR? may elicit the opposite effect.
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