老年阻塞性睡眠呼吸暂停综合征患者外周血单个核细胞核因子-κB的表达  

Activation and its influence of nuclear factor-κB in peripheral blood mononuclear cells in elderly patients with obstructive sleep apnea-hypopnea syndrome

作　　者：罗少华[1] 高兴林[1] 李东风[2] 吴健[1] 林琦[1] 欧琼[1] 李运雄[2] 岑瑞金[1] 杨晓霞[1] 

机构地区：[1]广东省人民医院东病区呼吸科广东省医学科学院广东省老年医学研究所,广州510080 [2]广东省医学科学院分子免疫学部

出　　处：《中华老年医学杂志》2010年第10期807-810,共4页Chinese Journal of Geriatrics

基　　金：广东省科技计划（2009B030801260）;广东省医学科研基金（B2009001）

摘　　要：目的 了解老年阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者中外周血单个核细胞（PBMC）的核因子-κB（NF-κB）活化及其致炎作用.方法 将40例老年患者（≥65岁）分为对照组、轻度OSAHS组、中度OSAHS组和重度OSAHS组（每组各10例）.所有对象于夜间行多导睡眠图仪检查,次晨采外周静脉血,分离PBMC,提取核蛋白,免疫印迹法测定NF-κB表达：酶联免疫吸附试验（ELISA）检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）浓度;对部分OSAHS患者（中、重度各5例）行4周每晚的持续气道正压通气（CPAP）治疗,治疗结束后复查上述指标.结果重度和中度OSAHS患者组PBMC NF-κB表达和血清TNF-α浓度均高于对照组,差异有统计学意义（P＜0.05）;各组血清IL-6浓度差异无统计学意义;PBMC NF-κB表达与呼吸暂停低通气指数（AHI）呈正相关（r=0.617,P＜0.001）,与夜间最低血氧饱和度（LSaO2）呈负相关（r=-0.548,P＜0.001）,与血清TNF-α浓度呈正相关（r=0.498,P＜0.001）,与血清IL-6浓度无相关关系（r=0.365,P=0.201）.CPAP可以抑制NF-κB活化（P＜0.001）,减少TNF-α分泌（P＜0.05）.结论 老年OSAHS患者PBMC可能通过活化NF-κB和分泌TNF-α,在血管内皮细胞损伤过程中发挥毒性作用,并与病情严重程度、夜间缺氧密切相关,但能被CPAP治疗有效抑制.Objective To evaluate the influence of nuclear factor （NF）-κB activation in peripheral blood mononuclear cells （PBMCs） on vascular inflammation in elderly patients with obstructive sleep apnea-hypopnea syndrome （OSAHS）. Methods The 40 elderly subjects （≥65years old） were classed into control, mild, moderate and severe groups （n = 10, respectively）according to polysomnography （PSG）. After PSG, the samples of peripheral venous blood were collected, and PBMCs were isolated. Nuclear protein was extracted and NF-κB was measured by Western blotting. ELISA was applied to measure the levels of TNF-α and IL-6 in serum. Blood samples from 10 cases （moderate 5 and severe 5） were measured again after four weeks of continuous positive airway pressure （CPAP） treatment. Results The expression of NF-κB in PBMCs and the concentration of TNF-α in serum were significantly increased in severe and moderate OSAHS patients compared with controls （P＜0. 05）. The NF-κB expression was positively correlated with AHI （r=0. 617, P＜ 0. 001） and TNF-α concentration （r = 0. 498, P＜ 0. 001 ）, negatively correlated with LSaO2 （r= -0. 548, P＜0. 001）, and not correlated with IL-6 concentration （r=0. 365, P=0. 201）.The CPAP treatment could significantly inhibit NF-κB activation in PBMCs and reduce TNF-αexcretion （P＜0.05, respectively）. Conclusions PBMCs may play an important role in vascular endothelial injury through NF-κB expression and TNF-α excretion in elderly OSAHS patients, which is closely associated with the severity of the syndrome and night hypoxemia. CPAP treatment can inhibit the pathophysiologic process effectively.

关 键 词：睡眠呼吸暂停 阻塞性 NF-ΚB 肿瘤坏死因子-Α 白细胞介素6 

分 类 号：R686[医药卫生—骨科学]