摘要来源： ann Transs Med。 2020年9月； 8（17）：1046。 PMID： 33145265”> 33145265
hanbo cao
摘要：
背景： 在当前的研究中，慢性髓样白血病（cml）细胞（CML）细胞（k562和ku812）与人类的骨骼相关（Bordssc），是人类的人类群体（boflyblys）。到伊马替尼（IM）。 CXCL12-CXCR4/7轴的激活在骨髓微环体的保护作用中起重要作用CML细胞上的NT（BME）。 The aim of this study was to investigate whether Wogonin could increase the sensitivity of CML cells to IM when they were co-cultured with BME and explore its underlying mechanism.
Methods: A model of CML cells co-cultured with BMSCs was applied. Flow cytometric, western blotting, immunofluorescence, and RT-PCR assays were used to explore the protective effects of BME on CML cells.
Results: The results showed that Wogonin could reverse the resistance of CML cells to IM under co-culture conditions by inhibiting Transforming growth factor-β （TGF-β）在BME中的分泌，防止SMAD4转移到核中，并随后降低CXCR4和CXCR7在CML细胞中的表达。此外，通过限制TGF-β/SMAD4/ID3途径，通过抑制CXCL12-CXCR4/7轴的激活来证明Wogonin的相反作用。s also showed that Wogonin decreased the expression of CXCR4 and CXCR7 in mice bone marrow with low systemic toxicity, and the mechanism was consistent with thestudy.
Conclusions: Wogonin increases the sensitivity of CML cells to IM in BME by controlling the TGF-β/SMAD4/ID3途径并降低CXCR4和CXCR7的表达。这些结果共同支持了Wogonin可能是治疗不耐CML的逆转剂的潜在候选者。