| 人脐带间充质干细胞改善地塞米松诱导的骨微血管内皮细胞凋亡 |
| hUCMSCs ameliorate dexamethasone-induced apoptosis of bone microvascular endothelial cells |
| 投稿时间：2024-09-29 |
| DOI：10.3969/j.issn.1672-5972.2025.02.008 |
| 中文关键词: 人脐带间充质干细胞 激素性股骨头坏死 骨微血管内皮细胞细胞 |
| 英文关键词:Human umbilical cord mesenchymal stem cells Steroid-induced osteonecrosis of the femoral head Bone microvascular endothelial cells |
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| 中文摘要: |
| 目的 探究人脐带间充质干细胞对地塞米松（Dex）干预下骨微血管内皮细胞细胞功能的影响。方法 分离并鉴定骨微血管内皮细胞并使用CCK8检测不同浓度Dex对骨微血管内皮细胞活力的影响，选取合适的Dex实验浓度处理骨微血管内皮细胞构建细胞模型，本实验分为空白组（单独培养BMECs）、Dex处理组（培养BMECs时加入地塞米松处理）、Dex+hUCMSC处理组（培养BMECs时加入地塞米松处理并与hUCMSC共培养）。通过细胞划痕实验和Transwell实验评估各组骨微血管内皮细胞迁移和侵袭能力；流式细胞仪检测和Western blot检测各组骨微血管内皮细胞中凋亡的发生情况。结果 ①本研究分离提取的原代细胞在免疫荧光检测中共表达CD31和VWF鉴定为BMECs。②CCK8检测结果显示Dex浓度达到200 μM时，显著抑制BMECs细胞活力，定为实验浓度。③划痕实验和Transwell实验：Dex干预下BMECs的迁移侵袭能力明显受到抑制，Dex+hUCMSC处理组中BMECs迁移侵袭能力受损低于Dex处理组。④Western blot和流式细胞仪凋亡检测：Dex显著诱导BMECs凋亡的发生。与hUCMSCs共培养后，Dex诱导的BMECs细胞凋亡得到一定程度逆转。结论 hUCMSCs能缓解地塞米松诱导的BMECs细胞凋亡，也能在一定程度上改善塞米松诱导的细胞功能损害。 |
| 英文摘要: |
| Objective To investigate the effect of hUCMSCs on Dex-induced bone microvascular endothelial cell (BMEC) function.Methods Bone microvascular endothelial cells were isolated and identified, and CCK8 was used to detect the effect of different concentrations of dexamethasone (Dex) on the viability of bone microvascular endothelial cells. The appropriate Dex experimental concentration was selected to treat bone microvascular endothelial cells to construct a cell model. The experiment was divided into blank group, Dex treatment group and Dex+hUCMSC treatment group(Blank group: BMECs cultured alone, Dex treatment group: BMECs cultured with dexamethasone, Dex+hUCMSC treatment group: BMECs cultured with dexamethasone and co-cultured with hUCMSC). The migration and invasion ability of bone microvascular endothelial cells in each group were evaluated by cell scratch test and Transwell test. Flow cytometry and Western blot were used to detect the apoptosis of bone microvascular endothelial cells in each group.Results ①The primary cells isolated and extracted in this study were identified as BMECs by immunofluorescence detection of co-expressing CD31 and VWF. ②The results of the CCK8 test showed that Dex at a concentration of 200 μM significantly inhibited the viability of BMECs, which was set as the experimental concentration. ③Scratch test and Transwell test: the migration and invasion ability of BMECs was significantly inhibited by Dex intervention, and the damage of migration and invasion ability of BMECs in Dex+hUCMSC treatment group was lower than that in Dex treatment group. ④Apoptosis detection by Western blot and flow cytometry: Dex significantly induced the occurrence of apoptosis in BMECs. After co-culture with hUCMSCs, the apoptosis of BMECs induced by Dex was partially reversed.Conclusion hUCMSCs can alleviate the apoptosis of BMECs induced by dexamethasone, and also ameliorate the cell function damage induced by dexamethasone to a certain extent. |
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