CAJ | 학술논문

目的：探讨重组人血管内皮抑素（ Endostar，恩度）对血管内皮细胞趋化、迁移、粘附、增殖及小管形成等与血管新生相关生物学行为的影响。方法以原代培养的人脐静脉内皮细胞（ HUVEC）为细胞模型，通过Boyden小室荧光定量分析、划痕试验、HUVEC荧光定量粘附分析、CFSE染色流式细胞术、CCK?8定量检测、小管形成试验和Matrigel栓试验研究恩度对HUVEC与血管新生相关的生物学行为的影响。结果恩度在5～50000ng／ml范围内可抑制血管内皮生长因子诱导HUVEC的迁移运动，且浓度为50ng／ml 和500ng／ml 时效果最明显；恩度在5～50000ng／ml间可呈剂量依赖的方式抑制HUVEC向损伤部位的迁移。与0ng／ml相比，50、500和5000ng／ml 恩度处理的HUVEC的粘附率、增殖率及HUVEC形成网状小管结构的数量、面积和长度均降低，差异均有统计学意义（ P＜0?05）； Matrigel栓实验结果显示，恩度在50～5000ng／ml间对SCID小鼠体内血管新生有明显的抑制作用。结论恩度在细胞水平能抑制HUVEC与血管新生相关的生物学行为，包括HU?VEC的趋化、迁移、粘附、增殖和小管形成；在动物水平能抑制SCID小鼠体内的血管新生，据此推断恩度能抑制血管新生。
목적：탐토중조인혈관내피억소（ Endostar，은도）대혈관내피세포추화、천이、점부、증식급소관형성등여혈관신생상관생물학행위적영향。방법이원대배양적인제정맥내피세포（ HUVEC）위세포모형，통과Boyden소실형광정량분석、화흔시험、HUVEC형광정량점부분석、CFSE염색류식세포술、CCK?8정량검측、소관형성시험화Matrigel전시험연구은도대HUVEC여혈관신생상관적생물학행위적영향。결과은도재5～50000ng／ml범위내가억제혈관내피생장인자유도HUVEC적천이운동，차농도위50ng／ml 화500ng／ml 시효과최명현；은도재5～50000ng／ml간가정제량의뢰적방식억제HUVEC향손상부위적천이。여0ng／ml상비，50、500화5000ng／ml 은도처리적HUVEC적점부솔、증식솔급HUVEC형성망상소관결구적수량、면적화장도균강저，차이균유통계학의의（ P＜0?05）； Matrigel전실험결과현시，은도재50～5000ng／ml간대SCID소서체내혈관신생유명현적억제작용。결론은도재세포수평능억제HUVEC여혈관신생상관적생물학행위，포괄HU?VEC적추화、천이、점부、증식화소관형성；재동물수평능억제SCID소서체내적혈관신생，거차추단은도능억제혈관신생。
Objective To study the effects of recombinant human endostatin( endostar) on the angiogenesis?related biological behaviors such as chemotaxis, migration, adhesion, proliferation and tube formation of vascular endothelial cells. Methods With pri?mary cultured human umbilical vein endothelial cells( HUVEC) as a model, the fluorescence quantitative Boyden chamber analysis, wound healing assay, fluorescence quantitative adhesion assay, flow cytometry, tube formation assay and Matrigel plug test were em?ployed to evaluate the effects of endostar on the angiogenesis?related biological behavior of HUVECs in vitro and in vivo. Results En?dostar potently inhibited HUVEC migration in response of VEGF from 50 to 50000ng/ml, and its significant concentrations were 50ng/ml and 500ng/ml. Endostar inhibited HUVEC migration towards damage between 50ng/ml and 50000ng/ml in a dose?dependent man?ner. Compared with 0ng/ml, the endostar at the dose of 50, 500 and 5000ng/ml decreased adhesion rate and proliferation rate of HU?VEC cells as well as the number, area and length of HUVEC mesh tubular with statistically significant difference( P<0?05) . Matrigel plug test also revealed that Endostar inhibited Matrigel plug formation in SCID mice between 50ng/ml and 50000ng/ml. Conclusion At the cellular level, endostar inhibited the angiogenesis?related biological behaviors of HUVECs, including migration, adhesion, pro?liferation and tube formation. In vivo, endostar inhibited the angiogenesis in SCID mice.