Rosiglitazone uppresses lipopolysaccharide-induced matrix metalloproteinase-2 activity in rat aortic endothelial cells via rasMEK1/2 signaling

作     者：WU Xiang-hong,LI Lang,MA Guo-tian,BI Qi,WEN wei-ming, XU Ge,LI Xing-san (Department of Cardiology,the First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China) 

出 版 物：《岭南心血管病杂志》 (South China Journal of Cardiovascular Diseases)

年 卷 期：2011年第17卷第S1期

页      面：193-193页

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

主　　题：MMPs MEK Rosiglitazone uppresses lipopolysaccharide-induced matrix metalloproteinase-2 activity in rat aortic endothelial cells via rasMEK1/2 signaling 

摘      要：ix metalloproteinase(MMPs) plays a key role in the pathogenesis of chronic inflammatory disease,such as *** MMPs,MMP-2 is regarded as a major proteinase in atherosclerotic plaque *** proliferator activated receptor-gamma(PPARg) ameliorates oxidative stress and the inflammatory *** aim of the present study was to evaluate the effect of Rosiglitazone on Lipopolysaccharide(LPS)-induced MMP-2 activation as well as its possible ***-induced MMP-2 activity was inhibited by Rosiglitazone(PPARg agonist) in the rat aortic endothelial cells(RAEC).LPS-induced MMP-2 activation was diminished no matter exposure to NF-kB Activation Inhibitor II(JSH-23)or Ras inhibitor,farnesylthiosalicylic acid(FTS). Further study shows that LPS-induced activation of Phospho-Rho A and Phospho-MEKl/2 were significantly inhibited by *** activation of NF-kB p65 in the nuclear extract of cells was also significantly suppressed by Rosiglitazone, moreover,the expression of NF-κB p65 was partly activated by GW9662(PPARg antagonist).NF-kB DNA binding activity was also demolished by *** summary,our data showed that PPARg agonist,Rosiglitazone suppresses LPS-activated MMP-2 secretion via Ras-MEK1/2 signaling pathways and NF-kB *** agonist and Ras-MEK1/2 pathway may be another potential therapeutic target for the disease induced by chronic inflammation.