Objective: To explore the influence of 1,4-benzoquinone (1,4-BQ) on proliferation of human bone marrow haematopoietic stem cells (hBM-HSCs) and human bone marrow mesenchymal stem cells (hBM-MSCs).
Methods: The bone marrow samples were collected from a healthy donor. Methylcellulose semi-solid culture medium was used to culture the mononuclear cells of bone marrow in different culture systems. Colony-forming unit (CFU) assay was utilized to evaluate the proliferation of hBM-HSCs exposed to 1,4-BQ at the doses of 10, 25, 50 and 100 µmol/L and to observe the influence of 1,4-BQ on the Colony-forming unit-erythroid (CFU-E)/Burst-forming unit-erythroid (BFU-E), Colony-forming unit-granulocyte, macrophage (CFU-GM), Colony-forming unit-granulocyte, erythroid, macrophage, megakaryocyte (CFU-GEMM) in hBM-MSCs. MTT assay was used to detect the proliferation of hBM-MSCs exposed to 1,4-BQ at the doses of 1, 5, 10, 25, 50, 100, 200, 500 and 1000 µmol/L for 24 h, respectively, after hBM-MSCs were isolated, cultured and expanded.
Results: The results of CFU assay indicated that numbers of CFU-E/BFU-E, CFU-GM and CFU-GEMM in 25, 50 and 100 µmol/L groups significantly decreased, as compared with control group (P < 0.05). However, no significant difference was found between the 10 µmol/L group and the control group. The results of MTT assay showed that the cellular viability of hBM-MSCs exposed to 1,4-BQ at the doses of 50 ∼ 200 µmol/L for 24 h significantly decreased in a dose-depended manner. When the exposure dose was higher than 200 µmol/L, the cellular viability of hBM-MSCs was lower than 5% which was significantly lower than that of control group (P < 0.05). When the exposure dose was lower than 25 µmol/L, there was no significant difference of cellular viability between exposure group and control group (P > 0.05).
Conclusion: The results of the present study demonstrated that 1,4-BQ could inhibit the colony forming of hBM-HSCs and the relative viability of hBM-MSCs in vitro. The hematotoxicity induced by 1,4-BQ may be related to inhibiting the proliferation capacity of hBM-HSCs.
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