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目的观察红花苷修复模拟微重力下人脐静脉内皮细胞(HUVECs)细胞迁移抑制的作用并探讨其机制。方法 MTT比色法选出红花苷干预HUVECs的最佳浓度;模拟失重-2D回转仪模拟失重培养HUVECs,分为正常重力对照组、模拟微重力组、红花苷微重力组。采用透膜侵袭小室模型检测细胞迁移;激光共聚焦显微镜观察红花苷干预后细胞骨架纤维状肌动蛋白(F-actin)的形态及对黏着斑(FAs)的影响。结果与正常重力对照组比较,模拟微重力组细胞迁移数下降(P<0.01);红花苷微重力组较模拟微重力组细胞迁移数增加(P<0.05)。正常重力对照组的F-actin呈现明显极化、微丝集结成束,模拟微重力可导致F-actin骨架重构,极化下降并呈现弥散特点;而红花苷微重力组的F-actin排列有序,伪足较模拟微重力组增多,方向性显著增强。模拟微重力组较正常重力对照组FAs数量(VN)、面积(VA)及FAs到细胞边缘距离(DS)显著降低(P<0.05);红花苷微重力组较模拟微重力组VN、VA、DS显著升高(P<0.05)。结论红花苷可改善模拟微重力作用导致的HUVECs迁移抑制,修复模拟微重力作用导致的HUVECs骨架F-actin的重构,改善FAs的生成及定位。
Objective To observe the effect of safflower glycoside on the migration inhibition of human umbilical vein endothelial cells (HUVECs) under simulated microgravity and explore its mechanism. Methods MTT colorimetric method was used to select the optimal concentrations of crocin to interfere with HUVECs. HUVECs were cultured with simulated weightlessness-2D rotameter and were divided into normal gravity group, simulated microgravity group and safranin microgravity group. Cell migration was detected by a transmembrane invasion chamber model. The morphology of F-actin and the effect on FAs were observed with laser confocal microscopy. Results Compared with the normal control group, the number of migrated cells in simulated microgravity group decreased (P <0.01). The migration of cells in simulated microgravity group increased significantly (P <0.05). F-actin in the normal gravity group showed obvious polarization and the filaments were aggregated into bundles. Simulated microgravity could lead to the remodeling of F-actin skeleton, actin arranged in order, pseudopodia than the simulated microgravity group increased, the direction was significantly enhanced. Compared with normal gravity control group, the number of FAs (VN), area (VA) and FAs to cell edge distance (DS) in simulated microgravity group were significantly decreased (P <0.05) , DS was significantly higher (P <0.05). CONCLUSION: Safflower glycosides can improve the migration inhibition of HUVECs induced by simulated microgravity, repair the remodeling of F-actin in HUVECs induced by simulated microgravity, and improve the formation and localization of FAs.