Fig 2: The mechanism of Quercetin or Licochalcone A in anti-AML. (A) Cell cycle analysis of AML cells treated with Quercetin reveals a strong increase in the G2-M cell population with a concomitant decrease in G1 population. (B) Cells treated with Quercetin at indicated concentrations for 24 h, whole-cell lysates were obtained and subjected to western blot analysis using antibodies against CDK1, phospho-CDK1 (p-CDK1), Cyclin A, Cyclin B1, GAPDH, (C) FACs analysis of CD11b and CD133 expression in AML cells lines treated with Quercetin. (D) Cells treated with Licochalcone A at indicated concentrations for 24 h, western blot analysis using antibodies against ERK1/2, phospho-ERK1/2 (p-ERK1/2), GAPDH. (E) Effects of Licochalcone A on morphology and differentiation of AML cells. Cells were treated with Licochalcone A and morphological changes were observed by phase contrast microscopy (mean ± SD, n.s, not significant, **p < 0.01, ***p < 0.001).

Fig 3: Post-I/R lymph upregulates neutrophil surface CD11b expression and facilitates neutrophil trans-endothelial migration. (A,B) Post-I/R lymph, but not pre-I/R lymph, upregulates surface CD11b expression on blood neutrophils (A) and on bone marrow derived neutrophils (B). n = 5–8/group. (C) Post-I/R lymph, but not pre-I/R lymph, promotes neutrophil trans-endothelial migration induced by recombinant CXCL1 (100 ng/mL). n = 6/group. *p < 0.05, **p < 0.01 vs. control. One-way ANOVA was used.

Fig 4: In vivo effects of monocytic EPOR knockout on bone cell precursors. Flow cytometry analysis of (a) preosteoclasts (CD115+) and (b) preosteoblasts (CD11b-Alp+) from the bone marrow of female LysMCreEPORf/f mice and their controls after treatment with either diluent or EPO. n = 8–12 in each group. * p < 0.05 versus diluent. All data are mean ± SEM. p values were calculated by 2-way ANOVA.

Fig 5: Microarray study data showing STAT6 and ß1-AR expression in CD11b+ myeloid cells of mice with MI. (A) The mRNA levels of STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6 in the splenic CD11b+ cells isolated from WT mice 1 week after MI. (B) The expression of ß1-AR in bone marrow and spleen-derived CD11b+ cells of WT mice. (C) The expression of ß1-AR in spleen-derived CD11b+ cells of WT mice after MI. (D) The expression of ß1-AR in spleen-derived CD11b+ cells of HDC-KO and WT mice after MI. (E) The expression of ß1-AR in bone marrow–derived CD11b+ cells of HDC-KO and WT mice after MI. ***P < 0.001, **P < 0.01, *P < 0.05. n = 5 per group.