中文摘要：

目的：测定不同程度间歇低氧（IH）处理的3T3-L1脂肪细胞中炎性细胞因子和脂肪因子水平的变化。方法建立阻塞性睡眠呼吸暂停（OSA）模式间歇低氧/再氧合（IH/ROX）细胞模型，将分化成熟的3T3-L1脂肪细胞分为5组，即3个不同程度IH组（5%O2，7.5%O2，10%O2，编号为IH-1，IH-2，IH-3）、持续低氧（10%O2，CH）组和正常氧对照（21%O2，IN）组。采用ELISA法测定脂肪细胞上清液中肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、瘦素和脂联素的水平，Western blot测定脂肪细胞中低氧诱导因子（HIF）-1α、葡萄糖转运蛋白（Glut）-1水平，Real-time-PCR测定脂肪细胞中HIF-1α、Glut-1、TNF-α、IL-6、瘦素、脂联素的mRNA表达水平。结果 IH组和CH组TNF-α、IL-6和瘦素蛋白及其mRNA水平均高于IN组，IH-1组TNF-α、IL-6和瘦素蛋白及瘦素mRNA水平高于IH-2、IH-3组（均P＜0.05）；IH组和CH组脂联素蛋白及其mRNA水平均低于IN组，IH-1组低于IH-2、IH-3组（均P＜0.05）。结论OSA模式IH与脂肪细胞炎性细胞因子和脂肪因子的表达和释放有关，IH可能是脂肪细胞炎症反应的基础，参与OSA患者胰岛素抵抗的发生。

英文摘要：

Objective To study the effect of different degrees of intermittent hypoxia （IH） on inflammatory cytokines and adipokines in 3T3-L1 adipocytes. Methods An intermittent hypoxia/reoxygenation （IH/ROX） from obstructive sleep apnea （OSA） adipocyte model was established. 3T3-L1 adipocytes were divided into five groups, three IH groups （5% O2, 7.5%O2 and 10%O2, referred to as IH-1, IH-2 and IH-3）, sustained hypoxia group （10%O2, CH） and the normal oxygen control group （21%O2, IN）. ELISA method was used to detect values of tumor necrosis factor alpha （TNF-α）, interleukin-6 （IL-6）, leptin and adiponectin in cell supernatant. Western blot analysis was used to detect levels of hypoxia-inducible fac-tor-1α（HIF-1α） and glucose transporter-1 （Glut-1）. RT-PCR assay was used to analyze HIF-1α, Glut-1, TNF-α, IL-6, leptin and adiponectin mRNA expression levels in adipocytes. Results The expression levels of TNF-α, IL-6 and leptin were significantly higher in IH and CH groups than those of IN group （P〈0.05）. The expression levels of TNF-α, IL-6 and leptin protein and leptin mRNA were significantly higher in IH-1 group than those of IH-2 and IH-3 groups （P〈0.05）. The adiponectin and its mRNA levels were significantly lower in IH and CH groups than those of IN group （P〈0.05）. The adipo-nectin level was significantly lower in IH-1 group than that of IH-2 and IH-3 groups （P〈0.05）. Conclusion These results demonstrate that IH is related to the extensive changes in the expression and release of inflammation-related adipokines in cultured adipocytes. IH from OSA may underlie the development of the inflammatory response in adipocytes, which is in-volved in insulin resistance in patients with OSA.