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10.3803/EnM.2017.32.1.115 http://scihub22266oqcxt.onion/10.3803/EnM.2017.32.1.115 C5368110!5368110!28256116     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28256116&cmd=llinks): Failed to open stream: HTTP request failed! 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Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor ? Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice |pdf=|usr=}}{{28256116}} gab.com Text Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice JO: Endocrinol Metab (Seoul) http://www.kidney.de/pget.php?&tw=1&pmid=28256116 #FOAvip Background: Renal tubulointerstitial fibrosis is a common feature of the final stage of nearly all cause types of chronic kidney disease. Although classic peroxisome proliferator-activated receptor ? (PPAR?) agonists have a protective effect on diabetic nephropathy, much less is known about their direct effects in renal fibrosis. This study aimed to investigate possible beneficial effects of lobeglitazone, a novel PPAR? agonist, on renal fibrosis in mice. Methods: We examined the effects of lobeglitazone on renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO) induced renal fibrosis mice. We further defined the role of lobeglitazone on transforming growth factor (TGF)-signaling pathways in renal tubulointerstitial fibrosis through in vivo and in vitro study. Results: Through hematoxylin/eosin and sirius red staining, we observed that lobeglitazone effectively attenuates UUO-induced renal atrophy and fibrosis. Immunohistochemical analysis in conjunction with quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that lobeglitazone treatment inhibited UUO-induced upregulation of renal Smad-3 phosphorylation, ?-smooth muscle actin, plasminogen activator inhibitor 1, and type 1 collagen. In vitro experiments with rat mesangial cells and NRK-49F renal fibroblast cells suggested that the effects of lobeglitazone on UUO-induced renal fibrosis are mediated by inhibition of the TGF-?/Smad signaling pathway. Conclusion: The present study demonstrates that lobeglitazone has a protective effect on UUO-induced renal fibrosis, suggesting that its clinical applications could extend to the treatment of non-diabetic origin renal disease. Twit Text FOAVip Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice ????Endocrinol Metab (Seoul) http://www.kidney.de/pget.php?&tw=1&pmid=28256116 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28256116 #FOAvip English Wikipedia <ref>{{Cite pmid|28256116}}</ref> Lobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor ? Agonist, Attenuates Renal Fibrosis Caused by Unilateral Ureteral Obstruction in Mice #MMPMID28256116 Bae KH; Seo JB; Jung YA; Seo HY; Kang SH; Jeon HJ; Lee JM; Lee S; Kim JG; Lee IK; Jung GS; Park KG Endocrinol Metab (Seoul) 2017[Mar]; 32 (1): 115-23 PMID28256116show ga Background: Renal tubulointerstitial fibrosis is a common feature of the final stage of nearly all cause types of chronic kidney disease. Although classic peroxisome proliferator-activated receptor ? (PPAR?) agonists have a protective effect on diabetic nephropathy, much less is known about their direct effects in renal fibrosis. This study aimed to investigate possible beneficial effects of lobeglitazone, a novel PPAR? agonist, on renal fibrosis in mice. Methods: We examined the effects of lobeglitazone on renal tubulointerstitial fibrosis in unilateral ureteral obstruction (UUO) induced renal fibrosis mice. We further defined the role of lobeglitazone on transforming growth factor (TGF)-signaling pathways in renal tubulointerstitial fibrosis through in vivo and in vitro study. Results: Through hematoxylin/eosin and sirius red staining, we observed that lobeglitazone effectively attenuates UUO-induced renal atrophy and fibrosis. Immunohistochemical analysis in conjunction with quantitative reverse transcription polymerase chain reaction and Western blot analysis revealed that lobeglitazone treatment inhibited UUO-induced upregulation of renal Smad-3 phosphorylation, ?-smooth muscle actin, plasminogen activator inhibitor 1, and type 1 collagen. In vitro experiments with rat mesangial cells and NRK-49F renal fibroblast cells suggested that the effects of lobeglitazone on UUO-induced renal fibrosis are mediated by inhibition of the TGF-?/Smad signaling pathway. Conclusion: The present study demonstrates that lobeglitazone has a protective effect on UUO-induced renal fibrosis, suggesting that its clinical applications could extend to the treatment of non-diabetic origin renal disease. äLobeglitazone, a Novel Peroxisome Proliferator-Activated Receptor ? Ag(epmc).pdf DeepDyve Pubget Overpricing