Introduction: To explore the molecular mechanism of YSSXG regulates myeloid hematopoietic cell proliferation and differentiation.
Materials and methods: Male Kun-Ming mice (n=52) were randomized into four groups (n=13): blank, model, positive drug, YSSXG. With the exception of blank group, all mice were irradiated with 60Co-γ rays (3.5 Gy). Two days prior to modeling, 3 g/kg YSSXG was administered intragastrically to mice in YSSXG group, while groups of blank, model and positive drug were administered with distilled water. The next day after modeling, mice in positive drug group were hypodermically injected with 30 μg/kg recombinant human granulocyte colony-stimulating factor; mice in the other groups received the same treatment as that prior to modeling, the duration of each course was 14 d. The contents of granulocytemacrophage colony stimulating factor (GM-CSF) in bone marrow supernatant and blood serum were assessed with radioimmunoassay. The mRNA expressions of GM-CSF and GM-CSF receptor alpha (GM-CSFRα) in bone marrow cells were analyzed by real-time fluorescent quantitative polymerase chain reaction. Protein expression of GM-CSF receptor beta (GM-CSFRβ) in bone marrow cell membranes was assayed via immunocytochemistry.
Results: YSSXG significantly increased GM-CSF contents in bone marrow supernatant and blood serum (all P<0.05), up-regulated mRNA expression of GM-CSF and GM-CSFRα in bone marrow cells (by 18.4 and 7.25 fold), and up-regulated GM-CSFRβ protein expression in cell membranes (P<0.05).
Discussion: The cell proliferation and differentiation of myeloid hematopoisis regulated by YSSXG were related to promoting the expressions of GM-CSF and GM-CSFR in bone marrow.