CAJ | 학술논문

目的：探讨脂肪细胞型脂肪酸结合蛋白（AFABP ）在糖尿病冠状动脉支架内再狭窄（ISR）中的作用。方法：在15头糖尿病猪和26头正常猪的冠状动脉内置入雷帕霉素洗脱支架，6个月后冠脉造影，选择正常和发生ISR 的血管段组织，提取蛋白进行定量二维荧光差异凝胶电泳技术（2D-DIGE ）和质谱检测。在人动脉平滑肌细胞（HASMC）中感染AFABP 的过表达和沉默病毒，检测细胞增殖、迁移能力和活性氧水平。结果：伴或不伴糖尿病的猪ISR 血管段组织内AFABP 水平均高于正常组织，且其在糖尿病ISR组织中高于非糖尿病ISR 组织。AFABP 过表达促进 HASMC 增殖和迁移，并伴有活性氧水平增高，上述效应在高糖培养基中更明显，抑制AFABP 表达能抑制这种效应。结论：AFABP在糖尿病冠状动脉ISR 血管段中表达显著增高；AFABP高表达促进动脉平滑肌细胞增殖和迁移，该效应可能由氧化应激介导。
목적：탐토지방세포형지방산결합단백（AFABP ）재당뇨병관상동맥지가내재협착（ISR）중적작용。방법：재15두당뇨병저화26두정상저적관상동맥내치입뢰파매소세탈지가，6개월후관맥조영，선택정상화발생ISR 적혈관단조직，제취단백진행정량이유형광차이응효전영기술（2D-DIGE ）화질보검측。재인동맥평활기세포（HASMC）중감염AFABP 적과표체화침묵병독，검측세포증식、천이능력화활성양수평。결과：반혹불반당뇨병적저ISR 혈관단조직내AFABP 수평균고우정상조직，차기재당뇨병ISR조직중고우비당뇨병ISR 조직。AFABP 과표체촉진 HASMC 증식화천이，병반유활성양수평증고，상술효응재고당배양기중경명현，억제AFABP 표체능억제저충효응。결론：AFABP재당뇨병관상동맥ISR 혈관단중표체현저증고；AFABP고표체촉진동맥평활기세포증식화천이，해효응가능유양화응격개도。
Objective:To investigate effects of adipocyte fatty acid binding protein (AFABP)on coronary artery in-stent restenosis (ISR )with diabetes. Methods:Rapamycin-eluting stents were implanted in the coronary arteries of 15 diabetic and 26 normal minipigs,and angiography was repeated after 6 months.The intima tissue of significant ISR and non-ISR segments in both diabetic and normal minipigs was analyzed by fluorescent two-dimensional difference gel electrophoresis (2D-DIGE)and mass spectrometry.AFABP overexpression and silencing virus were used to infect human arterial smooth muscle cells(HASMC),and cell proliferation,migration and the level of reactive oxygen species were detected. Results:AFABP levels were significantly increased in ISR tissue compared with non-ISR tissue in both diabetic and normal minipigs,and even higher in diabetic ISR tissue than that in non-diabetic ISR tissue.In HASMC,overexpression of AFABP significantly promoted proliferation and migration,and the effects were more prominent in high-glucose medium than those in low-glucose medium,whereas AFABP knockdown inhibited these effects. Conclusion:AFABP is significantly increased in coronary artery ISR segments of diabetic minipigs.Increased AFABP expression in HASMC promotes proliferation and migration possibly through reactive oxygen species-mediated activation.