CAJ | 학술논문

目的：通过建立大鼠心肌梗死模型，以流式细胞和免疫组化等方法探讨硝酸异山梨酯通过20－HETE调控内皮祖细胞促进血管新生的能力。方法：通过结扎冠脉前降支构建大鼠心肌梗死模型并给予ISDN及20－HETE特异性抑制剂（HET0016）干预8周，观察梗死面积、梗死交界区微血管密度及循环血中EPCs的数量。结果：ISDN有助于缩小心梗面积，增加梗死交界区微血管密度及循环血中的EPCs数量，20－HETE特异性抑制剂可部分阻断ISDN的效应。结论：ISDN可通过20－HETE调控EPCs促进血管新生。
목적：통과건립대서심기경사모형，이류식세포화면역조화등방법탐토초산이산리지통과20－HETE조공내피조세포촉진혈관신생적능력。방법：통과결찰관맥전강지구건대서심기경사모형병급여ISDN급20－HETE특이성억제제（HET0016）간예8주，관찰경사면적、경사교계구미혈관밀도급순배혈중EPCs적수량。결과：ISDN유조우축소심경면적，증가경사교계구미혈관밀도급순배혈중적EPCs수량，20－HETE특이성억제제가부분조단ISDN적효응。결론：ISDN가통과20－HETE조공EPCs촉진혈관신생。
Objective: To explore whether isosorbidedinitrate (ISDN) could promote angiogenesis through 20-HETE mediated-endothelial progenitor cells (EPCs) mobilization in a rat model of myocardial infarct. Methods:Experimental myocardial infarction (MI) model was established in rats via occlusion of the left anterior descending coronary artery. ISDN and a specific inhibitor of 20-HETE biosynthesis (HET0016) were administrated for eight weeks after MI surgery. Infarction area,microvascular density and the number of EPCs in the circulating blood were detected. Results:ISDN reduced the area of myocardial infarction, increased microvascular density in the border area of MI and the number of circulating EPCs in MI rats. However, 20-HETE biosynthesis inhibitor can partly block effect of ISDN. Conclusion: ISDN can promote angiogenesis by 20-HETE regulated-EPC smobilization.