Atorvastatin and NAC enhanced the quantity and function of cultivated BM EPCs from corticosteroid-resistant ITP patients via reducing p-p38 MAPK activity and inducing p-Akt activity. The cultivated BM EPCs from corticosteroid-resistant ITP patients were incubated with atorvastatin (ST; 500 nM), NAC (1 mM), SB203580 (10 μM), BIRB796 (400 nM), or ST (500 nM) combined with NAC (1 mM). The effects of the different treatments on (A) percentages (per well), (B) ROS levels, (C) double-positive–stained cells, (D) cell proliferation, (E) apoptosis, and (F) migration of cultivated BM EPCs from corticosteroid-resistant ITP patients were compared at day 7 in culture. (G) p-p38 and (H) p-Akt expression were analyzed by flow cytometry in the cultivated BM EPCs at day 7 in culture. (I) Representative western blots of p-p38, total p38, p-Akt, total Akt, and actin in the cultivated BM EPCs from corticosteroid-resistant ITP patients at day 7 in culture among the different treatments. The data were expressed as fold-change relative to corticosteroid-resistant ITP. Subject variables were compared using the Mann-Whitney U test for continuous variables. All P values <.05 were considered significant and were provided in the figure. BIRB796 and SB203580 indicate 2 kinds of p38 inhibitors.