ix metalloproteinase(MMPs) plays a key role in the pathogenesis of chronic inflammatory disease,such as atherosclerosis.Among MMPs,MMP-2 is regarded as a major proteinase in atherosclerotic plaque lesions.Peroxisome proliferator activated receptor-gamma(PPARg) ameliorates oxidative stress and the inflammatory response.The aim of the present study was to evaluate the effect of Rosiglitazone on Lipopolysaccharide(LPS)-induced MMP-2 activation as well as its possible mechanism.LPS-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 Rosiglitazone.The 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 Rosiglitazone.In summary,our data showed that PPARg agonist,Rosiglitazone suppresses LPS-activated MMP-2 secretion via Ras-MEK1/2 signaling pathways and NF-kB activation.PPARg agonist and Ras-MEK1/2 pathway may be another potential therapeutic target for the disease induced by chronic inflammation.
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机译:Retraction: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction. Dong‐Mei Wu, Yong‐Jian Wang, Xin‐Rui Han, Xin Wen, Lei Li, Lan Xu, Jun Lu and Yuan‐Lin Zheng. J Cell Mol Med. 2018; 22: 3058–3072 (https://doi.org/10.1111/jcmm.13557).
机译:Retraction: Tanshinone IIA prevents left ventricular remodelling via the TLR4/MyD88/NF‐κB signalling pathway in rats with myocardial infarction. Dong‐Mei Wu Yong‐Jian Wang Xin‐Rui Han Xin Wen Lei Li Lan Xu Jun Lu and Yuan‐Lin Zheng. J Cell Mol Med. 2018; 22: 3058–3072 (https://doi.org/10.1111/jcmm.13557).
机译:Eicosapentaenoic acid induces neovasculogenesis in human endothelial progenitor cells by modulating c-kit protein and pI3-K/akt/eNOs signaling pathways