河北医药
河北醫藥
하북의약
HEBEI MEDICAL JOURNAL
2013年
24期
3688-3690
,共3页
巨名飞%崔春燕%李金萍%张爱文%侯瑞田
巨名飛%崔春燕%李金萍%張愛文%侯瑞田
거명비%최춘연%리금평%장애문%후서전
阿托伐他汀%泡沫细胞%Lkn-1%氧化低密度脂蛋白%U937细胞系
阿託伐他汀%泡沫細胞%Lkn-1%氧化低密度脂蛋白%U937細胞繫
아탁벌타정%포말세포%Lkn-1%양화저밀도지단백%U937세포계
atorvastatin%foam cells%Lkn-1%oxidized low density lipoprotein%U937 cell line
目的:观察阿托伐他汀对ox-LDL诱导U937细胞形成泡沫细胞过程中Lkn-1表达的影响,探讨阿托伐他汀抗AS的作用机制。方法在由0.1μmol/L佛波脂( PMA)诱导分化人U937巨噬细胞中加入100 mg/Lox-LDL及不同浓度(0.1、1、10μmol/L)的阿托伐他汀共同孵育24 h,分别用酶联免疫吸附试验(ELISA)和RT-PCR方法检测培养细胞上清中Lkn-1的表达变化。结果 ox-LDL组较正常对照组Lkn-1的表达明显增加( P <0.05)。给药各组较ox-LDL组Lkn-1明显减少( P <0.05)。且随阿托伐他汀浓度的增加Lkn-1表达呈逐渐减少的趋势( P <0.05)。结论阿托伐他汀能抑制ox-LDL诱导U937细胞系形成泡沫细胞过程炎症因子Lkn-1的表达和分泌,可能为其抗动脉粥样硬化的重要机制之一。
目的:觀察阿託伐他汀對ox-LDL誘導U937細胞形成泡沫細胞過程中Lkn-1錶達的影響,探討阿託伐他汀抗AS的作用機製。方法在由0.1μmol/L彿波脂( PMA)誘導分化人U937巨噬細胞中加入100 mg/Lox-LDL及不同濃度(0.1、1、10μmol/L)的阿託伐他汀共同孵育24 h,分彆用酶聯免疫吸附試驗(ELISA)和RT-PCR方法檢測培養細胞上清中Lkn-1的錶達變化。結果 ox-LDL組較正常對照組Lkn-1的錶達明顯增加( P <0.05)。給藥各組較ox-LDL組Lkn-1明顯減少( P <0.05)。且隨阿託伐他汀濃度的增加Lkn-1錶達呈逐漸減少的趨勢( P <0.05)。結論阿託伐他汀能抑製ox-LDL誘導U937細胞繫形成泡沫細胞過程炎癥因子Lkn-1的錶達和分泌,可能為其抗動脈粥樣硬化的重要機製之一。
목적:관찰아탁벌타정대ox-LDL유도U937세포형성포말세포과정중Lkn-1표체적영향,탐토아탁벌타정항AS적작용궤제。방법재유0.1μmol/L불파지( PMA)유도분화인U937거서세포중가입100 mg/Lox-LDL급불동농도(0.1、1、10μmol/L)적아탁벌타정공동부육24 h,분별용매련면역흡부시험(ELISA)화RT-PCR방법검측배양세포상청중Lkn-1적표체변화。결과 ox-LDL조교정상대조조Lkn-1적표체명현증가( P <0.05)。급약각조교ox-LDL조Lkn-1명현감소( P <0.05)。차수아탁벌타정농도적증가Lkn-1표체정축점감소적추세( P <0.05)。결론아탁벌타정능억제ox-LDL유도U937세포계형성포말세포과정염증인자Lkn-1적표체화분비,가능위기항동맥죽양경화적중요궤제지일。
Objetc ive To observe the effect of atorvastatin ( AT) on the expression of Lkn-1 during U937 monocyte differentiating into foam cells induced by oxidized LDL ( ox-LDL) ,and to explore the antiatherosclerotic action mechanism of AT .Method s The macrophages derived from U 937 monocytes were induced by PMA (0.1μmol/L),which were treated with 100mg/L ox-LDL plus different concentrations of AT (0.1,1,10μmol/L) for 24 hours.Then the expression levels of Lkn-1 in supernatant of cultured cell were detected by ELISA and RT-PCR.Results As compared with those in control group ,the expression levels of Lkn-1 of in ox-LDL group were significantly increased ( P <0.05).However the expression levels of Lkn-1 in different concentrations of AT groups were significantly decreased ,as compared with those in ox-LDL group ( P <0.05).Moreover with the increase of AT concentration, the the expression levels of Lkn-1 were gradually decreased ( P <0.05 ). Conclusion Atorvastatin can inhibit the expression and secretion of Lkn-1 in the course of U937 monocyte differentiating into foam cells induced by ox-LDL,which may be the action mechanism of AT in anti-atherosclerosis and in inhibiting inflammatory factor .