IL-22在氧化型低密度脂蛋白损伤内皮细胞中的调节作用  

IL-22 is involved in atherosclerosis lesions by regulated impaired proliferation ability of oxidized low density lipoprotein treated CRL-1730

作　　者：孙懿[1] 韩志君[2] 黄元兰[3] 谷明莉[1] 陈燕[1] 胡志德[4] 邓安梅[1] 仲人前[3] 

机构地区：[1]第二军医大学长海医院实验诊断科,上海200433 [2]无锡市第二人民医院检验科,214002 [3]第二军医大学长征医院实验诊断科,上海200003 [4]济南军区总医院实验诊断科

出　　处：《中华微生物学和免疫学杂志》2012年第11期995-999,共5页Chinese Journal of Microbiology and Immunology

基　　金：国家自然科学基金（81072479,30672730,81170263）;上海市科委基金（09JC1405400）

摘　　要：目的研究氧化型低密度脂蛋白通过IL-22对人脐静脉内皮细胞（CRL-1730）增殖的影响及机制，初步探讨IL-22与冠状动脉粥样硬化（AS）发病机制的关系。方法采用RT-PCR检测8例无明显冠状动脉狭窄的健康个体和30例AS患者外周血单个核细胞（PBMC）IL-22mRNA的表达，ELISA法检测22例无明显冠状动脉狭窄的健康个体和79例AS患者血浆IL-22的浓度，分析IL-22的表达与AS患者冠状动脉最大狭窄程度及受累支数的关系。使用不同浓度氧化型低密度脂蛋白（OX—LDL）刺激CRL-1730细胞，24h后流式细胞术检测IL-22R1阳性细胞百分比。100μg/mlOX-LDL和20ng／mlIL-22共刺激CRL-1730细胞后，MTS法检测细胞的增殖能力，RT-PCR和ELISA检测碱性成纤维细胞生长因子（bFGF）的表达。结果随着患者冠状动脉狭窄程度和受累支数的增加，AS患者外周血PBMC中IL-22mRNA和血浆中IL-22水平逐渐降低。OX-LDL呈剂量依赖性地上调CRL-1730细胞中IL-22R1的表达。OX-LDL刺激可以引起CRL-1730细胞增殖能力受损、表达bFGF的能力降低，IL-22可以部分逆转OX—LDL的此种效应。结论IL-22可能具有抗AS的生物学效应，这种生物学效应可能与其拮抗OX-LDL对CRL-1730细胞增殖能力和表达bFGF的抑制作用有关。Objective To investigate the association between IL-22 and the pathogenesis of coro- nary artery atherosclerosis （AS）. Methods The relative expression of IL-22 mRNA in PBMC from 30 AS patients and 8 patients without any signs of coronary artery stenosis was detected by RT-PCR. Serum IL-22 levels of 22 patients without any signs of coronary artery stenosis and 79 AS patients were detected by ELISA. CRL-1730 cells（ human umbilical vein endothelial cells） were stimulated with oxidized low density lipoprotein （ox-LDL） at different dosage for 24 h, and the expression of IL-22R1 was detected by flowcytom- etry. The proliferation ability of CRL-1730 cells treated with IL-22（20 ng/ml） and/or ox-LDL（ 100 I^g/ml） was measured by MTS assay, and the expression of basic fibroblast growth factor（bFGF） was detected by RT- PCR and ELISA. Results Decreased IL-22 expression in PBMC and serum was observed as worsen of AS. The expression of IL-22R1 in ox-LDL treated CRL-1730 cells was increased in dose dependent manner. Ox- LDL decreased proliferation ability, as well as bFGF expression and releasing, of CRL-1730 ceils. This effect of ox-LDL was partially rescued by IL-22. Conclusion IL-22 may have anti-atherosclerosis effect. This effect may be mediated by regulating bFGF expression and endothelial cells proliferation ability in the pres- ence of IL-22.

关 键 词：动脉粥样硬化 白细胞介素22 人脐静脉内皮细胞 氧化型低密度脂蛋白 增殖 碱 性成纤维细胞生长因子 

分 类 号：R541.4[医药卫生—心血管疾病]