Acute myelod leukemia (AML), as a uncontrolled proliferation of cells, was arrested differentiation of progenitor cells. The present study aimed to explore Tanshinone IIA (TIIA) effects on OCI-AML3 and the involvement of the MAPK signaling pathway and miR-497 in TIIA-mediated effects. Cell growth percentage was detected using a cell counting kit. Expression of miR-497 was detected by qPCR. Phosphorylated ERK1/2, JNK and p38 were assessed using western blot. The growth percentage of OCI-AML3 decreased and the effected time increased with increasing TIIA concentration. The miR-497 was upregulated and the p-ERK1/2 was decreased when the TIIA added. TIIA cannot influence the p-ERK1/2. Hence, the proliferation of OCI-AML3 cells was raising. However, when the p-ERK1/2 was inhibited, there no influence on the miR-497 expression after TIIA added. TIIA upregulates miR-497, and decrease the p-ERK1/2 expression, when TIIA simulated OCI-AML3 cell in vitro. And in miR-497 might be involved in the regulation of proliferation in this process.

中文翻译：

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miR-497通过MAPK / ERK1 / 2途径在丹参酮IIA减弱OCI-AML3细胞增殖中起关键作用。

急性骨髓性白血病（AML）作为不受控制的细胞增殖，被阻止了祖细胞的分化。本研究旨在探讨丹参酮IIA（TIIA）对OCI-AML3的作用以及MAPK信号通路和miR-497在TIIA介导的作用中的作用。使用细胞计数试剂盒检测细胞生长百分比。通过qPCR检测miR-497的表达。使用蛋白质印迹法评估磷酸化的ERK1 / 2，JNK和p38。随着TIIA浓度的增加，OCI-AML3的生长百分比降低，且作用时间增加。加入TIIA后，miR-497上调，p-ERK1 / 2降低。TIIA不能影响p-ERK1 / 2。因此，OCI-AML3细胞的增殖正在增加。但是，当p-ERK1 / 2被抑制时，加入TIIA后对miR-497的表达没有影响。当TIIA体外模拟OCI-AML3细胞时，TIIA上调miR-497，并降低p-ERK1 / 2表达。而miR-497可能参与了此过程中的增殖调控。