依达拉奉对骨髓基质干细胞氧化损伤的调节作用

背景：既往依达拉奉作为抗氧化剂对神经细胞氧化损伤的保护作用已得到证实，但其对骨髓基质干细胞氧化损伤的保护作用未见明确报道及深入研究。 目的：观察依达拉奉对骨髓基质干细胞在氧化损伤中的调节作用。 方法：通过冲洗髓腔的方法提取新西兰大耳白兔的长骨骨髓，然后应用密度梯度离心联合贴壁筛选的方法体外培养获得骨髓基质干细胞。实验将第3代骨髓基质干细胞分为5组：空白组仅加入体积分数为10%胎牛血清、1%的双抗的低糖DMEM培养液；地塞米松组加入含有1×10-7 mol/L地塞米松的细胞培养液，不含有依达拉奉；50，100，300 mg/L依达拉奉组分别加入1×10-7 mol/L的地塞米松和质量浓度为50，100，300 mg/L的依达拉奉，培养后分别用四甲基偶氮唑蓝法、流式细胞仪法检测细胞增殖水平及细胞周期。 结果与结论：依达拉奉组较空白组及地塞米松组细胞增殖水平明显增强，依达拉奉对骨髓基质干细胞起到了保护作用，当依达拉奉质量浓度为50 mg/L时即发挥作用(P < 0.05)，并且与依达拉奉的质量浓度有一定的量效关系，当依达拉奉质量浓度为100 mg/L时，其保护作用明显提高(P < 0.01)，但随着质量浓度的增加，这种保护作用没有进一步增加，反而稍有下降。结果表明：高浓度地塞米松可以使骨髓基质干细胞受到氧化损伤，依达拉奉可以通过抗氧化作用保护骨髓基质干细胞免受氧化损伤。中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程全文链接：

Edaravone protects bone marrow stromal cells from oxidative injury

BACKGROUND: Edaravone as an antioxidant protective effect on nerve cells injured by hydrogen peroxide has been confirmed, but its protective effect on oxidative damage to bone marrow stromal cells has not been reported in-depth. OBJECTIVE: To investigate the regulatory effects of edaravone on oxidative injury to bone marrow stromal cells. METHODS:Bone marrow samples were extracted from the long bone of New Zealand rabbits by the method of washing the pulp cavity, then subjected to the density gradient centrifugation and adherent screening to obtain bone marrow stromal stem cells in vitro. The bone marrow stromal cells at 3 passage were divided into five groups: blank group, treated with low-glucose Dulbecco’s modified Eagle’s medium containing 10% fetal bovine serum and 1% double antibody; dexamethasone group, treated with cell culture medium containing 1×10-7 mol/L dexamethasone; 50, 100, 300 mg/L edaravone groups, cultured in cell culture medium containing 1×10-7 mol/L dexamethasone and 50, 100, 300 mg/L edaravone, respectively. After culture, MTT method and flow cytometry were used to detect the proliferative level and cell cycle of cells. RESULTS AND CONCLUSION: Compared with the control and dexamethasone groups, edaravone significantly enhanced the cell proliferation. Edaravone played a protective role in bone marrow stromal cells. When the concentration was 50 mg/L, edaravone began to play a regulatory role (P < 0.05), and this effect was certainly associated with the concentration of edaravone. When the concentration was up to 100 mg/L, edaravone showed a better protective role (P < 0.01). However, with increasing concentration, this protective effect was not further increased, but decreased slightly. Results indicated that high-concentration dexamethasone can induce oxidative injury to bone marrow stromal cells, and edaravone can protect the cells against this oxidative damage by antioxidant role.