Low-dose decitabine inhibited the STAT3 signaling pathway. (A) Representative western blots of phosphorylated-STAT3 (p-STAT3), total STAT, phosphorylated-AKT (p-AKT), total AKT, and GAPDH in PBMCs from patients with ITP before and after decitabine treatment. (B-C) Graphs present densitometry data of relative phosphorylated protein to total protein (n = 3). Treg cells in CD4⁺ T cells from healthy control subjects (D; n = 10) and patients with ITP (E; n = 8) in the STAT3 inhibitor plus decitabine group were no different from those in the STAT3 inhibitor group in vitro. In the presence of AKT inhibitor, decitabine significantly increased the percentage of Treg cells from patients with ITP in vitro (G; n = 10), but not in the healthy control subjects (F; n = 8). (H) The platelet counts in the STAT3 inhibitor plus decitabine group were not significantly different from those in mice receiving STAT3 inhibitor (n = 6). (I) AKT inhibitor plus decitabine increased platelet counts in mice compared with AKT inhibitor on day 21 (n = 6). *P < .05. Dec, decitabine; ns, not significant.