Gao Hui-Qiang, Xu Shang-Dong, Li Jiang-Rong, Zheng Jun, Sun Li-Zhong
Department of Cardiovascular Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, and Beijing Engineering Research Center of Vascular Prostheses, Beijing, China.
Department of Cardiovascular Surgery, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, and Beijing Engineering Research Center of Vascular Prostheses, Beijing, China.
Transplant Proc. 2020 Jan-Feb;52(1):419-422. doi: 10.1016/j.transproceed.2019.10.007. Epub 2020 Jan 14.
In the design and development of small-caliber artificial blood vessels, endothelialization is a key issue, but it is not well understood at present. Some studies have used vascular endothelial growth factor (VEGF) sustained-release methods to promote endothelial cell proliferation. However, this method is not ideal. This study has used drugs to induce endothelial cells to produce VEGF. This method in turn functions to promote cell proliferation and promote the endothelialization of artificial blood vessels. This study aimed to investigate the effect of the antiplatelet drug tirofiban on endothelial cell proliferation in vitro.
In this study, human umbilical vein endothelial cells (HUVECs) were used to determine the effect of tirofiban-stimulated cell proliferation. Analysis of cell proliferation, assayed by the Cell Counting Kit-8 assay, showed that the number of cells was increasingly higher than in the absence of tirofiban. It was also observed that heparin enhanced the tirofiban effect. The cell VEGF expression at different time points after tirofiban addition was detected by western blot analysis.
The absorbance values of the experimental (1 μg/mL tirofiban) and the control groups (0 tirofiban) were 1.74 (SD, 0.03) and 1.51 (SD, 0.07) (P < .001), respectively, after 4 days of culture under the same conditions. The amount of VEGF produced by HUVECs gradually increased after treatment with tirofiban, reached a peak at 2 hours, and was 1.3-fold greater than the control group (P = .034). Compared with the tirofiban-only group, the absorbance value of the tirofiban and 10 μg/mL of heparin group was significantly increased (P < .001).
Tirofiban promoted the proliferation of HUVECs by promoting the synthesis of VEGF in HUVECs. Heparin enhanced tirofiban activity in promoting HUVEC proliferation.
在小口径人工血管的设计与研发中，内皮化是一个关键问题，但目前对此尚未完全了解。一些研究采用血管内皮生长因子（VEGF）缓释方法来促进内皮细胞增殖。然而，这种方法并不理想。本研究采用药物诱导内皮细胞产生VEGF。该方法进而起到促进细胞增殖和推动人工血管内皮化的作用。本研究旨在探讨抗血小板药物替罗非班对体外内皮细胞增殖的影响。
在本研究中，使用人脐静脉内皮细胞（HUVECs）来确定替罗非班刺激细胞增殖的效果。通过细胞计数试剂盒-8检测法对细胞增殖进行分析，结果显示细胞数量比未使用替罗非班时逐渐增多。还观察到肝素可增强替罗非班的作用效果。通过蛋白质印迹分析检测添加替罗非班后不同时间点细胞VEGF的表达情况。
在相同条件下培养4天后，实验组（1μg/mL替罗非班）和对照组（0μg/mL替罗非班）的吸光度值分别为1.74（标准差，0.03）和1.51（标准差，0.07）（P <.001）。用替罗非班处理后，HUVECs产生的VEGF量逐渐增加，在2小时达到峰值，比对照组高1.3倍（P =.034）。与仅使用替罗非班的组相比，替罗非班与10μg/mL肝素组的吸光度值显著增加（P <.001）。
替罗非班通过促进HUVECs中VEGF的合成来促进其增殖。肝素增强了替罗非班促进HUVEC增殖的活性。
