1 Ocak 2014 Dergi makalesi Açık Erişim

Sari, A. Nihal; Kacan, Meltem; Unsal, Demet; Firat, Seyhan Sahan; Buharalioglu, C. Kemel; Vezir, Ozden; Korkmaz, Belma; Cuez, Tuba; Canacankatan, Necmiye; Sucu, Nehir; Ayaz, Lokman; Gumus, Lulufer Tamer; Gorur, Aysegul; Tunctan, Bahar

Dublin Core

<?xml version='1.0' encoding='utf-8'?>
<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Sari, A. Nihal</dc:creator>
  <dc:creator>Kacan, Meltem</dc:creator>
  <dc:creator>Unsal, Demet</dc:creator>
  <dc:creator>Firat, Seyhan Sahan</dc:creator>
  <dc:creator>Buharalioglu, C. Kemel</dc:creator>
  <dc:creator>Vezir, Ozden</dc:creator>
  <dc:creator>Korkmaz, Belma</dc:creator>
  <dc:creator>Cuez, Tuba</dc:creator>
  <dc:creator>Canacankatan, Necmiye</dc:creator>
  <dc:creator>Sucu, Nehir</dc:creator>
  <dc:creator>Ayaz, Lokman</dc:creator>
  <dc:creator>Gumus, Lulufer Tamer</dc:creator>
  <dc:creator>Gorur, Aysegul</dc:creator>
  <dc:creator>Tunctan, Bahar</dc:creator>
  <dc:date>2014-01-01</dc:date>
  <dc:description>The small G protein RhoA and its downstream effector Rho-kinase play an important role in various physiopathological processes including ischemia/reperfusion (I/R) injury. Reactive oxygen and nitrogen species produced by iNOS and NADPH oxidase are important mediators of inflammation and organ injury following an initial localized I/R event. The aim of this study was to determine whether RhoA/Rho-kinase signaling pathway increases the expression and activity of MEK1, ERK1/2, iNOS, gp91(phox), and p47(phox), and peroxynitrite formation which result in oxidative/nitrosative stress and inflammation leading to hindlimb PR-induced injury in kidney as a distant organ and;,gastrocnemius muscle as a target organ. I/R-induced distant and target organ injury was performed by using the rat hindlimb tourniquet model, I/R caused an increase in the expression and/or activity of RhoA, MEK1, ERK1/2, iNOS, gp91(phox), p47(phox), and 3-nitrotyrosine and nitrotyrosine levels in the tissues. Although Rho-kinase activity was increased by I/R in the kidney, its activity was decreased in the muscle. Serum and tissue MDA levels and MPO activity were increased following I/R. PR also caused an increase in SOD and catalase activities associated with decreased GSH levels in the tissues. Y-27632, a selective Rho-kinase inhibitor, (100 mu g/kg, i.p.; 1 h before reperfusion) prevented the I/R-induced changes except Rho-kinase activity in the muscle. These results suggest that activation of RhoA/Rho-kinase/MEK1/ERK1/2/iNOS pathway associated with oxidative/nitrosative stress and inflammation contributes to hindlimb PR-induced distant organ injury in rats. It also seems that hindlimb I/R induces target organ injury via upregulation of RhoA/MEK1/ERK1/2/iNOS pathway associated with decreased Rho-kinase activity. (C) 2013 Elsevier B.V. All rights reserved.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/65705</dc:identifier>
  <dc:identifier>oai:zenodo.org:65705</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>EUROPEAN JOURNAL OF PHARMACOLOGY 723 234-245</dc:source>
  <dc:title>Contribution of RhoA/Rho-kinase/MEK1/ERK1/2/iNOS pathway to ischemia/reperfusion-induced oxidative/nitrosative stress and inflammation leading to distant and target organ injury in rats</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>