Polydatin (PD), a natural precursor of resveratrol, has a variety of biological activities, including anticancer effects. However, the molecular mechanisms underlying the anticancer activity of polydatin have not been fully elucidated. In this study, we demonstrated that PD significantly inhibited the proliferation of the MOLT-4 leukemic cell line in a dose- and time-dependent manner using the Cell Counting Kit-8 assay.
Polydatin also dose-dependently increased the apoptotic rate and caused S-phase cell cycle arrest in MOLT-4 cells, as revealed by flow cytometry. In addition, PD dose-dependently decreased mitochondrial membrane potential and led to the generation of reactive oxygen species in MOLT-4 cells. Western blot analysis revealed that the expression of anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein was decreased, whereas that of pro-apoptotic Bcl-2-associated X protein was increased by PD.
In addition, the expression of two cell cycle regulatory proteins, cyclin D1 and cyclin B1, was suppressed by polydatin. Of note, the pro-apoptotic and cell cycle inhibitory effects of PD were enhanced by inhibition of Janus kinase 2 (JAK2). In conclusion, the results of this scientific research strongly suggested that polydatin is a promising therapeutic compound for the treatment of leukemia, particularly in combination with JAK inhibitors..
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