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10.1038/s41598-017-12285-8 http://scihub22266oqcxt.onion/10.1038/s41598-017-12285-8 C5607272!5607272 !28931916     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28931916 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2017 ; 7 (1 ): 12026 Nephropedia Template TP {{tp|p=28931916 |t=2017. Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF-?B and HMGB1 pathways through the upregulation of SIRT1 |pdf=|usr=}}{{28931916 }} gab.com Text Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF- B and HMGB1 pathways through the upregulation of SIRT1 JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28931916 #FOAvip Sepsis is a life-threatening medical condition. Salidroside, a substance isolated from Rhodiola rosea, possesses antioxidant and anti-inflammatory properties. The effect and mechanism of salidroside on sepsis-induced acute lung injury still remains to be well clarified. Here, we investigated the effect and mechanism of salidroside on septic mouse models and explored the role of salidroside-upregulated SIRT1. Salidroside inhibited the inflammatory responses and HMGB1 productions in bacterial lipopolysaccharide (LPS)-treated macrophages and mice. Salidroside could also reverse the decreased SIRT1 protein expression in LPS-treated macrophages and mice. Salidroside also alleviated the sepsis-induced lung edema, lipid peroxidation, and histopathological changes and the mortality, and improved the lung PaO(2)/FiO(2) ratio in cecal ligation and puncture (CLP)-induced septic mice. Salidroside significantly decreased the serum TNF-?, IL-6, NO, and HMGB1 productions, pulmonary inducible NO synthase (iNOS) and phosphorylated NF-?B-p65 protein expressions, and pulmonary HMGB1 nuclear translocation in CLP septic mice. Moreover, sepsis decreased the SIRT1 protein expression in the lungs of CLP septic mice. Salidroside significantly upregulated the SIRT1 expression and inhibited the inflammatory responses in CLP septic mouse lungs. These results suggest that salidroside protects against sepsis-induced acute lung injury and mortality, which might be through the SIRT1-mediated repression of NF-?B activation and HMGB1 nucleocytoplasmic translocation. Twit Text FOAVip Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF- B and HMGB1 pathways through the upregulation of SIRT1 ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28931916 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28931916 #FOAvip English Wikipedia <ref>{{Cite pmid|28931916 }}</ref> Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF-?B and HMGB1 pathways through the upregulation of SIRT1 #MMPMID28931916 Lan KC ; Chao SC ; Wu HY ; Chiang CL ; Wang CC ; Liu SH ; Weng TI Sci Rep 2017[Sep]; 7 (1 ): 12026 PMID28931916 show ga Sepsis is a life-threatening medical condition. Salidroside, a substance isolated from Rhodiola rosea, possesses antioxidant and anti-inflammatory properties. The effect and mechanism of salidroside on sepsis-induced acute lung injury still remains to be well clarified. Here, we investigated the effect and mechanism of salidroside on septic mouse models and explored the role of salidroside-upregulated SIRT1. Salidroside inhibited the inflammatory responses and HMGB1 productions in bacterial lipopolysaccharide (LPS)-treated macrophages and mice. Salidroside could also reverse the decreased SIRT1 protein expression in LPS-treated macrophages and mice. Salidroside also alleviated the sepsis-induced lung edema, lipid peroxidation, and histopathological changes and the mortality, and improved the lung PaO(2)/FiO(2) ratio in cecal ligation and puncture (CLP)-induced septic mice. Salidroside significantly decreased the serum TNF-?, IL-6, NO, and HMGB1 productions, pulmonary inducible NO synthase (iNOS) and phosphorylated NF-?B-p65 protein expressions, and pulmonary HMGB1 nuclear translocation in CLP septic mice. Moreover, sepsis decreased the SIRT1 protein expression in the lungs of CLP septic mice. Salidroside significantly upregulated the SIRT1 expression and inhibited the inflammatory responses in CLP septic mouse lungs. These results suggest that salidroside protects against sepsis-induced acute lung injury and mortality, which might be through the SIRT1-mediated repression of NF-?B activation and HMGB1 nucleocytoplasmic translocation. |Acute Lung Injury/etiology/metabolism/*prevention & control [MESH] |Animals [MESH] |Down-Regulation/drug effects [MESH] |Glucosides/*pharmacology [MESH] |HMGB1 Protein/*metabolism [MESH] |Macrophages/drug effects/metabolism [MESH] |Male [MESH] |Mice [MESH] |NF-kappa B/*metabolism [MESH] |Phenols/*pharmacology [MESH] |Phytotherapy [MESH] |RAW 264.7 Cells [MESH] |Rhodiola/chemistry [MESH] |Sepsis/*complications [MESH] |Signal Transduction/drug effects [MESH] |Sirtuin 1/*metabolism [MESH]Salidroside ameliorates sepsis-induced acute lung injury and mortality(epmc).pdf DeepDyve Pubget Overpricing