动物实验,FOXO3A z-bo 2020-09-11 368

　　Objective: To study the effect of FOXO3A gene knockout mice on hematopoietic ionizing radiation (IR) damage?

　　Methods: FOXO3A-/- mice and wild-type mice (FVB/N) were divided into small wild-type mice mouse control group (WT group) and FOXO3A-/- mouse control group (FOXO3A-/- group) , Wild mouse irradiation group (WT IR), FOXO3A-/- mouse irradiation group (FOXO3A-/- IR) these four groups received false irradiation and 4Gy X-ray whole body irradiation (TBI), and Dose rate. Is it 0.9 Gy/min? FOXO3A-/- mice and WT mice were tested 14 days after receiving organ index, peripheral blood and TBI. Observation of FOXO3A gene knockout on bone marrow cell count, bone marrow cell typing, hematopoietic progenitor cell (HPC) granulocyte macrophage colony forming unit (colony forming unit-granulocyte and macrophage, CFU-GM) forming ability and hematopoietic radiation Can you be affected by the injury?

　　Results: Under physiological conditions, the number of bone marrow nucleated cells in FOXO3A-/- mice decreased, and the proportion of HPC increased (P\u003c0.05); the mice received 4 GyX-ray TBI treatments for 14 days and the FOXO3A gene was knocked out It exacerbates the HPC induced by ionizing radiation and reduces the proportion of hematopoietic stem cells (HSC), which also reduces the number of CFU of radiation-induced myeloid nucleated cells and hematopoietic progenitor cells. Do you suppress the reduction in transgene formation?

　　Conclusion: FOXO3A gene knockout can maintain homeostasis and deteriorate the hematopoietic system. Does radiation damage to mouse HPC and HSC have a specific effect on the radiosensitivity of hematopoietic cells? The role of FOXO3A in regulating hematopoietic ionizing radiation damage and whether it can be used as a target for prevention and treatment of damage needs further consideration.