Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1155/2015/691070 http://scihub22266oqcxt.onion/10.1155/2015/691070 C4442292!4442292 !26078813     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 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\26078813 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oxid+Med+Cell+Longev 2015 ; 2015 (ä): 691070 Nephropedia Template TP {{tp|p=26078813 |t=2015. Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis |pdf=|usr=}}{{26078813 }} gab.com Text Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=26078813 #FOAvip Hydrogen sulfide (H2S) is a gasotransmitter which regulates multiple cardiovascular functions. However, the precise roles of H2S in modulating myocardial fibrosis in vivo and cardiac fibroblast proliferation in vitro remain unclear. We investigated the effect of GYY4137, a slow-releasing H2S donor, on myocardial fibrosis. Spontaneously hypertensive rats (SHR) were administrated with GYY4137 by intraperitoneal injection daily for 4 weeks. GYY4137 decreased systolic blood pressure and inhibited myocardial fibrosis in SHR as evidenced by improved cardiac collagen volume fraction (CVF) in the left ventricle (LV), ratio of perivascular collagen area (PVCA) to lumen area (LA) in perivascular regions, reduced hydroxyproline concentration, collagen I and III mRNA expression, and cross-linked collagen. GYY4137 also inhibited angiotensin II- (Ang II-) induced neonatal rat cardiac fibroblast proliferation, reduced the number of fibroblasts in S phase, decreased collagen I and III mRNA expression and protein synthesis, attenuated oxidative stress, and suppressed ?-smooth muscle actin (?-SMA), transforming growth factor-?1 (TGF-?1) expression as well as Smad2 phosphorylation. These results indicate that GYY4137 improves myocardial fibrosis perhaps by a mechanism involving inhibition of oxidative stress, blockade of the TGF-?1/Smad2 signaling pathway, and decrease in ?-SMA expression in cardiac fibroblasts. Twit Text FOAVip Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=26078813 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26078813 #FOAvip English Wikipedia <ref>{{Cite pmid|26078813 }}</ref> Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis #MMPMID26078813 Meng G ; Zhu J ; Xiao Y ; Huang Z ; Zhang Y ; Tang X ; Xie L ; Chen Y ; Shao Y ; Ferro A ; Wang R ; Moore PK ; Ji Y Oxid Med Cell Longev 2015[]; 2015 (ä): 691070 PMID26078813 show ga Hydrogen sulfide (H2S) is a gasotransmitter which regulates multiple cardiovascular functions. However, the precise roles of H2S in modulating myocardial fibrosis in vivo and cardiac fibroblast proliferation in vitro remain unclear. We investigated the effect of GYY4137, a slow-releasing H2S donor, on myocardial fibrosis. Spontaneously hypertensive rats (SHR) were administrated with GYY4137 by intraperitoneal injection daily for 4 weeks. GYY4137 decreased systolic blood pressure and inhibited myocardial fibrosis in SHR as evidenced by improved cardiac collagen volume fraction (CVF) in the left ventricle (LV), ratio of perivascular collagen area (PVCA) to lumen area (LA) in perivascular regions, reduced hydroxyproline concentration, collagen I and III mRNA expression, and cross-linked collagen. GYY4137 also inhibited angiotensin II- (Ang II-) induced neonatal rat cardiac fibroblast proliferation, reduced the number of fibroblasts in S phase, decreased collagen I and III mRNA expression and protein synthesis, attenuated oxidative stress, and suppressed ?-smooth muscle actin (?-SMA), transforming growth factor-?1 (TGF-?1) expression as well as Smad2 phosphorylation. These results indicate that GYY4137 improves myocardial fibrosis perhaps by a mechanism involving inhibition of oxidative stress, blockade of the TGF-?1/Smad2 signaling pathway, and decrease in ?-SMA expression in cardiac fibroblasts. |Actins/metabolism [MESH] |Angiotensin II/toxicity [MESH] |Animals [MESH] |Blood Pressure/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Cells, Cultured [MESH] |Collagen Type I/genetics/metabolism [MESH] |Collagen Type II/genetics/metabolism [MESH] |Fibroblasts/cytology/drug effects/metabolism [MESH] |Heart Ventricles/metabolism [MESH] |Heart/*drug effects [MESH] |Hydroxyproline/metabolism [MESH] |Male [MESH] |Morpholines/*pharmacology [MESH] |Myocardium/metabolism/*pathology [MESH] |Organothiophosphorus Compounds/*pharmacology [MESH] |Oxidative Stress/drug effects [MESH] |Rats [MESH] |Rats, Inbred SHR [MESH] |Rats, Sprague-Dawley [MESH] |Rats, Wistar [MESH] |Reactive Oxygen Species/metabolism [MESH] |Smad2 Protein/metabolism [MESH]Hydrogen Sulfide Donor GYY4137 Protects against Myocardial Fibrosis (epmc).pdf DeepDyve Pubget Overpricing