CAJ | 학술논문

目的：探讨血管紧张素转换酶2（ACE2）基因转染对内皮细胞血凝素样氧化型低密度脂蛋白受体-1(LOX-1)表达的影响及意义。方法：实验包括体外实验与体内实验。体外实验，首先进行人脐静脉内皮细胞（HUVEC）的培养，然后应用蛋白质印迹法检测ACE2转染对血管紧张素II刺激HUVEC产生的LOX-1蛋白表达的影响。体内实验，首先建立载脂蛋白E基因敲除(ApoE-/-)小鼠动脉粥样硬化模型。然后将20只ApoE-/-小鼠随机分为ACE2组及增强型绿色荧光蛋白组（EGFP组），每组10只。ACE2组经尾静脉注射ACE2的复制缺陷重组腺病毒（Ad-ACE2）(2.5×109 pfu/ml)，EGFP组注射等量EGFP的复制缺陷重组腺病毒(Ad-EGFP)。注射一个月后处死动物，做腹主动脉的油红O及LOX-1表达的检测。结果：体内实验与体外实验均证实ACE2基因转染抑制了内皮细胞LOX-1的表达，体内实验中ACE2组斑块内脂质含量明显低于EGFP组水平。结论：ACE2通过抑制LOX-1的表达进而抑制了动脉粥样硬化斑块的进展。
목적：탐토혈관긴장소전환매2（ACE2）기인전염대내피세포혈응소양양화형저밀도지단백수체-1(LOX-1)표체적영향급의의。방법：실험포괄체외실험여체내실험。체외실험，수선진행인제정맥내피세포（HUVEC）적배양，연후응용단백질인적법검측ACE2전염대혈관긴장소II자격HUVEC산생적LOX-1단백표체적영향。체내실험，수선건립재지단백E기인고제(ApoE-/-)소서동맥죽양경화모형。연후장20지ApoE-/-소서수궤분위ACE2조급증강형록색형광단백조（EGFP조），매조10지。ACE2조경미정맥주사ACE2적복제결함중조선병독（Ad-ACE2）(2.5×109 pfu/ml)，EGFP조주사등량EGFP적복제결함중조선병독(Ad-EGFP)。주사일개월후처사동물，주복주동맥적유홍O급LOX-1표체적검측。결과：체내실험여체외실험균증실ACE2기인전염억제료내피세포LOX-1적표체，체내실험중ACE2조반괴내지질함량명현저우EGFP조수평。결론：ACE2통과억제LOX-1적표체진이억제료동맥죽양경화반괴적진전。
Objective: To investigate the inlfuence of angiotensin converting enzyme 2 (ACE2) on lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) protein expression and to explore the protective effect of ACE2 on vascular endothelial cells. Methods: Our work includedin vitro andin vivo studies. For in vitro experiment, the human umbilical vein endothelial cell (HUVEC) were cultured and transfected with replication deficient recombinant adenovirus of ACE2 (Ad-ACE2), and LOX-1 protein expression stimulated by angiotensin 2 was examined by Western blot analysis. Forin vivo study, atherosclerosis plaques were induced in 20 apolipoprotein E-deifcient (ApoE-/-) mice, and then randomly divided them into 2 groups: ACE2 group, the mice received Ad-ACE2 (2.5×109 pfu/ml) injection through caudal vein, EGFP (enhanced green lfuorescent protein) group, the mice received equal replication deifcient recombinant adenovirus of EGFP (Ad-EGFP) injection through caudal vein.n=10 in each group. The animals were executed after 1 month treatment to collect abdominal aorta. Lipid content in atherosclerosis plaque was evaluated by Oil red O staining and LOX-1 protein expression was examined by immunohistochemistry and Western blot analysis. Results: Bothin vitro andin vivo experiments conifrmed that endothelial cell LOX-1 protein expression was signiifcantly inhibited by ACE2 transfection. The lipid content in ACE2 group was obviously lower than that in EGFP group byin vivo study. Conclusion: ACE2 may inhibit LOX-1 protein expression and therefore reduce the progress of atherosclerosis.