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http://scihub22266oqcxt.onion/ C4637590!4637590!26617775     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26617775&cmd=llinks): Failed to open stream: HTTP request failed! 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Fenofibrate, a PPAR? agonist, protect proximal tubular cells from albumin-bound fatty acids induced apoptosis via the activation of NF-kB |pdf=|usr=}}{{26617775}} gab.com Text Fenofibrate, a PPAR agonist, protect proximal tubular cells from albumin-bound fatty acids induced apoptosis via the activation of NF-kB JO: Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26617775 #FOAvip Albumin-bound fatty acids is the main cause of renal damage, PPAR? is responsible in the metabolism of fatty acids. Previous study found that PPAR? played a protective role in fatty acids overload associated tubular injury. The aim of the present study is to investigate whether fenofibrate, a PPAR? ligands, could contribute to the renoprotective action in fatty acids overload proximal tubule epithelial cells. We observed in HK-2 cells that fenofibrate significantly inhibited fatty acids bound albumin (FA-BSA) induced up-regulation of MCP-1 and IL-8. Treatment with fenofibrate attenuated renal oxidative stress induced by FA-BSA as evidenced by decreased MDA level, increased SOD activity and catalase, GPx-1 expression. FA-BSA induced apoptosis of HK-2 cells were also obviously prevented by fenofibrate. Furthermore, fenofibrate significantly increased the expression of PPAR? mRNA and protein in FA-BSA treated cells. Finally, the activation of NF-kB induced by FA-BSA was markedly suppressed by fenofibrate. Taken together, our study describes a renoprotective role of fenofibrate in fatty acids associated tubular toxicity, and the transcriptional activation of PPAR? and suppression of NF-kB were at least partially involved. Twit Text FOAVip Fenofibrate, a PPAR agonist, protect proximal tubular cells from albumin-bound fatty acids induced apoptosis via the activation of NF-kB ????Int J Clin Exp Pathol http://www.kidney.de/pget.php?&tw=1&pmid=26617775 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26617775 #FOAvip English Wikipedia <ref>{{Cite pmid|26617775}}</ref> Fenofibrate, a PPAR? agonist, protect proximal tubular cells from albumin-bound fatty acids induced apoptosis via the activation of NF-kB #MMPMID26617775 Zuo N; Zheng X; Liu H; Ma X Int J Clin Exp Pathol 2015[]; 8 (9): 10653-61 PMID26617775show ga Albumin-bound fatty acids is the main cause of renal damage, PPAR? is responsible in the metabolism of fatty acids. Previous study found that PPAR? played a protective role in fatty acids overload associated tubular injury. The aim of the present study is to investigate whether fenofibrate, a PPAR? ligands, could contribute to the renoprotective action in fatty acids overload proximal tubule epithelial cells. We observed in HK-2 cells that fenofibrate significantly inhibited fatty acids bound albumin (FA-BSA) induced up-regulation of MCP-1 and IL-8. Treatment with fenofibrate attenuated renal oxidative stress induced by FA-BSA as evidenced by decreased MDA level, increased SOD activity and catalase, GPx-1 expression. FA-BSA induced apoptosis of HK-2 cells were also obviously prevented by fenofibrate. Furthermore, fenofibrate significantly increased the expression of PPAR? mRNA and protein in FA-BSA treated cells. Finally, the activation of NF-kB induced by FA-BSA was markedly suppressed by fenofibrate. Taken together, our study describes a renoprotective role of fenofibrate in fatty acids associated tubular toxicity, and the transcriptional activation of PPAR? and suppression of NF-kB were at least partially involved. �Fenofibrate, a PPAR? agonist, protect proximal tubular cells from albu(epmc).pdf DeepDyve Pubget Overpricing