中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
CHINESE JOURNAL OF MICROBIOLOGY AND IMMUNOLOGY
2012年
11期
995-999
,共5页
孙懿%韩志君%黄元兰%谷明莉%陈燕%胡志德%邓安梅%仲人前
孫懿%韓誌君%黃元蘭%穀明莉%陳燕%鬍誌德%鄧安梅%仲人前
손의%한지군%황원란%곡명리%진연%호지덕%산안매%중인전
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
動脈粥樣硬化%白細胞介素22%人臍靜脈內皮細胞%氧化型低密度脂蛋白%增殖%堿性成纖維細胞生長因子
동맥죽양경화%백세포개소22%인제정맥내피세포%양화형저밀도지단백%증식%감성성섬유세포생장인자
Atherosclerosis%Interleukin-22%Human umbilical vein endothelial cell%Oxidized low density lipoprotein%Proliferation%Basic fibroblast growth factor
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-22 mRNA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,24 h后流式细胞术检测IL-22R1阳性细胞百分比.100 μg/ml ox-LDL和20 ng/ml IL-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-22 mRNA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,IL42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.
目的 研究氧化型低密度脂蛋白通過IL-22對人臍靜脈內皮細胞(CRL-1730)增殖的影響及機製,初步探討IL-22與冠狀動脈粥樣硬化(AS)髮病機製的關繫.方法 採用RT-PCR檢測8例無明顯冠狀動脈狹窄的健康箇體和30例AS患者外週血單箇覈細胞(PBMC) IL-22 mRNA的錶達,ELISA法檢測22例無明顯冠狀動脈狹窄的健康箇體和79例AS患者血漿IL-22的濃度,分析IL-22的錶達與AS患者冠狀動脈最大狹窄程度及受纍支數的關繫.使用不同濃度氧化型低密度脂蛋白(ox-LDL)刺激CRL-1730細胞,24 h後流式細胞術檢測IL-22R1暘性細胞百分比.100 μg/ml ox-LDL和20 ng/ml IL-22共刺激CRL-1730細胞後,MTS法檢測細胞的增殖能力,RT-PCR和ELISA檢測堿性成纖維細胞生長因子(bFGF)的錶達.結果 隨著患者冠狀動脈狹窄程度和受纍支數的增加,AS患者外週血PBMC中IL-22 mRNA和血漿中IL-22水平逐漸降低.ox-LDL呈劑量依賴性地上調CRL-1730細胞中IL-22R1的錶達.ox-LDL刺激可以引起CRL-1730細胞增殖能力受損、錶達bFGF的能力降低,IL42可以部分逆轉ox-LDL的此種效應.結論 IL-22可能具有抗AS的生物學效應,這種生物學效應可能與其拮抗ox-LDL對CRL-1730細胞增殖能力和錶達bFGF的抑製作用有關.
목적 연구양화형저밀도지단백통과IL-22대인제정맥내피세포(CRL-1730)증식적영향급궤제,초보탐토IL-22여관상동맥죽양경화(AS)발병궤제적관계.방법 채용RT-PCR검측8례무명현관상동맥협착적건강개체화30례AS환자외주혈단개핵세포(PBMC) IL-22 mRNA적표체,ELISA법검측22례무명현관상동맥협착적건강개체화79례AS환자혈장IL-22적농도,분석IL-22적표체여AS환자관상동맥최대협착정도급수루지수적관계.사용불동농도양화형저밀도지단백(ox-LDL)자격CRL-1730세포,24 h후류식세포술검측IL-22R1양성세포백분비.100 μg/ml ox-LDL화20 ng/ml IL-22공자격CRL-1730세포후,MTS법검측세포적증식능력,RT-PCR화ELISA검측감성성섬유세포생장인자(bFGF)적표체.결과 수착환자관상동맥협착정도화수루지수적증가,AS환자외주혈PBMC중IL-22 mRNA화혈장중IL-22수평축점강저.ox-LDL정제량의뢰성지상조CRL-1730세포중IL-22R1적표체.ox-LDL자격가이인기CRL-1730세포증식능력수손、표체bFGF적능력강저,IL42가이부분역전ox-LDL적차충효응.결론 IL-22가능구유항AS적생물학효응,저충생물학효응가능여기길항ox-LDL대CRL-1730세포증식능력화표체bFGF적억제작용유관.
Objective To investigate the association between IL-22 and the pathogenesis of coronary 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 flowcytometry.The proliferation ability of CRL-1730 cells treated with IL-22(20 ng/ml) and/or ox-LDL(100 μg/ml)was measured by MTS assay,and the expression of basic fibroblast growth factor(bFGF) was detected by RTPCR 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.OxLDL decreased proliferation ability,as well as bFGF expression and releasing,of CRL-1730 cells.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 presence of IL-22.