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Haiyan Zhao,Yaping Zhao,Xin Li,Leiqian Xu,Fangxin Jiang,Wanju Hou,Lixia Dong,Jie Cao 연세대학교의과대학 2018 Yonsei medical journal Vol.59 No.9
Purpose: Obstructive sleep apnea and chronic obstructive pulmonary disease are independent risk factors of cardiovascular disease(CVD), and their coexistence is known as overlap syndrome (OS). Endothelial dysfunction is the initial stage of CVD; however,underlying mechanisms linking OS and CVD are not well understood. The aim of this study was to explore whether OS canlead to more severe inflammation and endothelial apoptosis by promoting endothelial dysfunction, and to assess the interventioneffects of antioxidant tempol. Materials and Methods: Male Wistar rats (n=66) were exposed to normal oxygen [normal control (NC) group], intermittent hypoxia(IH group), cigarette smoke (CH group), as well as cigarette smoke and IH (OS group). Tempol intervention was assessed inOS group treated with tempol (OST group) or NaCl (OSN group). After an 8-week challenge, lung tissues, serum, and fresh bloodwere harvested for analysis of endothelial markers and apoptosis. Results: The levels of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, and apoptosis in circulating epithelialcells were the highest in OS group and the lowest in NC group. These levels were all greater in IH group than in CH group,and were lower in OST group than in OS and OSN groups (all p<0.001). Conclusion: Synergistic effects of IH with cigarette smoke-induced emphysema produce a greater inflammatory status and endothelialapoptosis. OS-related inflammation and endothelial cell apoptosis may play important roles in promoting cardiovasculardysfunction, and antioxidant tempol could achieve a partial protective effect.