Zhao Haiyan, Zhao Yaping, Li Xin, Xu Leiqian, Jiang Fangxin, Hou Wanju, Dong Lixia, Cao Jie
Respiratory Department of Tianjin Medical University General Hospital, Tianjin, China.
Respiratory Department of Tianjin Medical University General Hospital Airport Hospital, Tianjin, China.
Yonsei Med J. 2018 Nov;59(9):1079-1087. doi: 10.3349/ymj.2018.59.9.1079.
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 can lead to more severe inflammation and endothelial apoptosis by promoting endothelial dysfunction, and to assess the intervention effects of antioxidant tempol.
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 in OS group treated with tempol (OST group) or NaCl (OSN group). After an 8-week challenge, lung tissues, serum, and fresh blood were harvested for analysis of endothelial markers and apoptosis.
The levels of intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, and apoptosis in circulating epithelial cells 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 <0.001).
Synergistic effects of IH with cigarette smoke-induced emphysema produce a greater inflammatory status and endothelial apoptosis. OS-related inflammation and endothelial cell apoptosis may play important roles in promoting cardiovascular dysfunction, and antioxidant tempol could achieve a partial protective effect.
阻塞性睡眠呼吸暂停和慢性阻塞性肺疾病是心血管疾病（CVD）的独立危险因素，二者并存被称为重叠综合征（OS）。内皮功能障碍是心血管疾病的初始阶段；然而，OS与CVD之间的潜在机制尚不清楚。本研究的目的是探讨OS是否通过促进内皮功能障碍导致更严重的炎症和内皮细胞凋亡，并评估抗氧化剂Tempol的干预效果。
将雄性Wistar大鼠（n = 66）暴露于正常氧气环境[正常对照组（NC组）]、间歇性缺氧（IH组）、香烟烟雾（CH组）以及香烟烟雾加间歇性缺氧（OS组）。在接受Tempol治疗的OS组（OST组）或NaCl治疗的OS组（OSN组）中评估Tempol干预效果。经过8周的刺激后，采集肺组织、血清和新鲜血液，用于分析内皮标志物和细胞凋亡情况。
细胞间黏附分子-1、血管细胞黏附分子-1的水平以及循环上皮细胞中的细胞凋亡情况在OS组中最高，在NC组中最低。这些水平在IH组中均高于CH组，在OST组中低于OS组和OSN组（均P<0.001）。
间歇性缺氧与香烟烟雾诱导的肺气肿的协同作用产生更严重的炎症状态和内皮细胞凋亡。OS相关的炎症和内皮细胞凋亡可能在促进心血管功能障碍中起重要作用，抗氧化剂Tempol可起到部分保护作用。
