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10.1371/journal.pone.0151986 http://scihub22266oqcxt.onion/10.1371/journal.pone.0151986 C4807015!4807015!27010330     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27010330&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 253.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2016 ; 11 (3): ä Nephropedia Template TP {{tp|p=27010330|t=2016. Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-?1/Smad Signaling Pathway |pdf=|usr=}}{{27010330}} gab.com Text Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF- 1/Smad Signaling Pathway JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27010330 #FOAvip Transforming growth factor-?1 (TGF-?1) signaling has been shown to play a critical role in the development of diabetic nephropathy (DN). The nuclear transcription co-repressor Ski-related novel protein N (SnoN) is an important negative regulator of TGF-?1/Smad signal transduction, and subsequent biological responses including tubule epithelial-mesenchymal transition (EMT), extracellular matrix accumulation and tubulointerstitial fibrosis. Oxymatrine (OM) is an alkaloid extracted from the Chinese herb Sophora japonica and has been demonstrated to prevent fibrosis. However, the anti-fibrosis effect of OM in DN is still unclear. In this study, we cultured normal rat renal tubular epithelial cells (NRK52Es) in high glucose and high glucose plus OM, and detected the expression of E-cadherin, ?-SMA, FN, TGF-?1, SnoN, Arkadia, p-Smad2 and p-Smad3 and poly-ubiquitination of SnoN. The results showed that E-cadherin and SnoN expression in NRK52Es decreased significantly, but poly-ubiquitination of SnoN, TGF-?1, ?-SMA, FN, Arkadia, p-Smad2 and p-Smad3 expression significantly increased due to high glucose stimulation, which could be almost completely reversed by OM, suggesting that OM may alleviate EMT induced by high glucose via upregulating SnoN expression and inhibiting TGF-?1/Smad signaling pathway activation. Hence, OM could be a novel therapeutic for DN. Twit Text FOAVip Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF- 1/Smad Signaling Pathway ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27010330 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27010330 #FOAvip English Wikipedia <ref>{{Cite pmid|27010330}}</ref> Oxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upregulation of SnoN and Inhibition of TGF-?1/Smad Signaling Pathway #MMPMID27010330 Liu L; Wang Y; Yan R; Li S; Shi M; Xiao Y; Guo B PLoS One 2016[]; 11 (3): ä PMID27010330show ga Transforming growth factor-?1 (TGF-?1) signaling has been shown to play a critical role in the development of diabetic nephropathy (DN). The nuclear transcription co-repressor Ski-related novel protein N (SnoN) is an important negative regulator of TGF-?1/Smad signal transduction, and subsequent biological responses including tubule epithelial-mesenchymal transition (EMT), extracellular matrix accumulation and tubulointerstitial fibrosis. Oxymatrine (OM) is an alkaloid extracted from the Chinese herb Sophora japonica and has been demonstrated to prevent fibrosis. However, the anti-fibrosis effect of OM in DN is still unclear. In this study, we cultured normal rat renal tubular epithelial cells (NRK52Es) in high glucose and high glucose plus OM, and detected the expression of E-cadherin, ?-SMA, FN, TGF-?1, SnoN, Arkadia, p-Smad2 and p-Smad3 and poly-ubiquitination of SnoN. The results showed that E-cadherin and SnoN expression in NRK52Es decreased significantly, but poly-ubiquitination of SnoN, TGF-?1, ?-SMA, FN, Arkadia, p-Smad2 and p-Smad3 expression significantly increased due to high glucose stimulation, which could be almost completely reversed by OM, suggesting that OM may alleviate EMT induced by high glucose via upregulating SnoN expression and inhibiting TGF-?1/Smad signaling pathway activation. Hence, OM could be a novel therapeutic for DN. äOxymatrine Inhibits Renal Tubular EMT Induced by High Glucose via Upre(epmc).pdf DeepDyve Pubget Overpricing