TY - JOUR T1 -肺功能正常吸烟者rho激酶表达和活性升高及肺内皮功能障碍JF - European Respiratory Journal JO - Eur Respir J SP - 349 LP - 355 DO - 10.1183/09031936.00056610 VL - 37 IS - 2 AU - Duong-Quy, S. AU - Dao, P. AU - Hua-Huy, T. AU - Guilluy, C. AU - Pacaud, P. AU - Dinh-Xuan，A.T. Y1 - 2011/02/01 UR - //www.qdcxjkg.com/content/37/2/349.abstract N2 -内皮功能障碍是香烟烟雾对血管系统的毒性作用的主要后果之一。越来越多的证据表明，小g蛋白RhoA及其下游效应物RhoA激酶(ROCKs)参与了香烟烟雾引起的系统性内皮功能障碍。本研究旨在评估RhoA/ROCKs通路在肺功能正常的吸烟者肺动脉内皮功能中的作用。肺组织取自非吸烟者和因肺癌接受肺叶切除术的吸烟者。在孤立的肺动脉环中评估乙酰胆碱(ACh)反应的动脉舒张。观察内皮型一氧化氮合酶(eNOS)、ROCKs和肌球蛋白磷酸酶亚基1 (MYPT-1)的蛋白表达和活性。与非吸烟者相比，吸烟者对ACh的反应放松显著降低(每组n = 8)，与前者的eNOS活性降低相一致。然而，eNOS蛋白表达在两组中保持一致。与对照组相比，吸烟组ROCKs、鸟苷三磷酸rhoa和磷酸化MYPT-1的表达显著增加。 Pulmonary endothelial dysfunction is present in smokers whose lung function has not yet been impaired. Reduced activity of eNOS accounts at least in part for this endothelial dysfunction. Increased expression and activity of ROCKs accounts for another part through direct or indirect inhibition of the Rho-A/ROCKs pathway on nitric oxide synthesis and sustained pulmonary vasoconstriction through inhibition of myosin phosphatase. ER -