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  • Title: [EFFECT OF MACROPHAGE MIGRATION INHIBITORY FACTOR ON VASCULAR REPAIR OF STEROID-INDUCED AVASCULAR NECROSIS OF FEMORAL HEAD IN VITRO].
    Author: Ma J, Zhang C, Zhang E, Ban W, Lü L, Dang X, Wang K.
    Journal: Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi; 2016 Aug 08; 30(8):998-1005. PubMed ID: 29786232.
    Abstract:
    OBJECTIVE: To interpret the mechanisms of vascular repair disorders in steroid-induced avascular necrosis of the femoral head (SANFH) via detection of the changes of proliferation, migration, and macrophage migration inhibitory factor (MIF)/vascular endothelial growth factor (VEGF) expressions of endothelial cells (ECs) under hypoxia/glucocorticoid. METHODS: According to culture conditions, human umbilical vein ECs (HUVECs) at passage 3 were divided into group A (normal), group B (1.0×10-6 mol/L dexamethasone), group C (hypoxia), and group D (hypoxia+1.0×10-6 mol/L dexamethasone). The cell activity was detected by AlamarBlue; the number of viable cells was detected in live/dead cell staining; the cell morphology was observed after cytoskeleton staining; cell migration ability was compared by scratch test; and the levels of MIF and VEGF expressions were detected by ELISA. RESULTS: At 24 hours after culture, the cell activity and the number of living cells in group C were significantly higher than those in the other 3 groups, showing significant difference between groups (P<0.05), and group D had the worst cell activity and least living cells. Cytoskeleton staining showed that cells had normal morphology in groups A and B; cells had rich cytoskeleton and secretion granules in group C; cytoskeleton form disorder and nucleus pyknosis were observed in group D. Scratch test showed that the cell migration ability of group C was strongest while cell migration ability of group D was weakest. Accumulated concentration of MIF and VEGF in 4 groups significantly increased with time extending. Accumulated concentration of MIF in group C were significantly higher than that in other 3 groups at each time point (P<0.05). Within 24 hours after intervention, stage concentration of MIF during 1-8 hours was significantly lower than that during 0-1 hour and 8-24 hours in every group (P<0.05). Stage concentration of MIF in group C was significantly higher than other groups during 0-1 hour and 8-24 hours (P<0.05). Within 2 hours after intervention, stage concentration of MIF in 4 groups during 0.5-1 hour was significantly higher than that during other stages (P<0.05). Accumulated concentration of VEGF in group C was significantly higher than that in other groups at 8 and 24 hours (P<0.05). The stage concentration of VEGF in groups C and D during 8-24 hours was significantly higher than that during 0-1 hour and 1-8 hours (P<0.05). There was no significant difference in the stage concentration of VEGF within and among group A, B, C, and D at every stage within 2 hours after intervention (P>0.05). CONCLUSIONS: In hypoxia environment, the proliferation and migration of ECs is enhanced, and the secretion of VEGF and MIF is increased. High concentration of dexamethasone will suppress the process above, which induces vascular repair disorders and aggravating SANFH. 目的: 通过检测体外缺氧/激素作用下内皮细胞（endothelial cells，ECs）增殖、迁徙以及巨噬细胞移动抑制因子（macrophage migration inhibitory factor，MIF）和VEGF的表达变化，探讨激素性股骨头缺血性坏死（steroid-induced avascular necrosis of femoral head，SANFH）血管修复障碍发生机制。. 方法: 取第3代人脐静脉ECs（human umbilical vein ECs，HUVECs）进行分组干预。正常对照组（A组）细胞不作任何干预；地塞米松组（B组）：用含1.0×10-6 mol/L地塞米松的完全培养液干预；缺氧培养组（C组）：细胞在低氧细胞培养罐内培养；地塞米松+缺氧培养组（D组）：细胞在低氧细胞培养罐内培养，同时用含1.0×10-6 mol/L地塞米松的完全培养液干预。干预培养后24 h，行AlamarBlue细胞活性检测及活/死细胞染色观测细胞增殖情况，细胞骨架染色观察细胞骨架形态；采用划痕实验比较各组细胞迁徙能力，ELISA法检测各组细胞MIF及VEGF表达水平。. 结果: 干预培养后24 h，AlamarBlue细胞活性检测及活/死细胞染色示C组细胞活性最好且活细胞数多，D组细胞活性最差、活细胞数最少，组间比较差异均有统计学意义（P＜0.05）。细胞骨架染色见，A、B组细胞形态正常；C组细胞大量增殖，细胞内见大量分泌颗粒；D组细胞骨架形态异常。划痕实验示C组细胞迁移能力最强，D组最弱。各组MIF和VEGF累积浓度随时间延长均显著增高。各时间点，C组MIF累积浓度显著高于其他各组（P＜0.05）。干预培养24 h内，各组组内1～8 h时MIF阶段浓度显著低于0～1 h及8～24 h时（P＜0.05）；且C组0～1 h和8～24 h时MIF阶段浓度显著高于其他组（P＜0.05）。干预培养2 h内，各组组内0.5～1 h MIF阶段浓度显著高于其他各时间段（P＜0.05）。8、24 h时C组VEGF累积浓度显著高于其他各组（P＜0.05）。干预24 h内，C、D组8～24 h时VEGF阶段浓度显著高于其他各时间段（P＜0.05）；干预培养2 h内，各组组内各时间段及组间VEGF阶段浓度比较，差异均无统计学意义（P＞0.05）。. 结论: 缺氧条件下ECs增殖及迁徙能力增强，MIF及VEGF分泌增加；而高浓度地塞米松会抑制上述过程，引发血管修复障碍，导致SANFH发生、发展。.
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