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探讨了致死性中子辐射后重组人白介素11(Recombinanthumaninterleukin?11,rhIL?11)对小鼠骨髓损伤的防治作用及其机制。采用二级雄性BALB/c小鼠96只,分别于4.0Gy中子全身照射前3d或后3d皮下注射rhIL?11,于照射后6h、1d和2d活杀取材,计数外周血和骨髓有核细胞。采用核仁组成区嗜银蛋白(ArgyrophilicofNucleaolarorganizerregions,AgNOR)染色检测骨髓细胞核嗜银蛋白含量、流式细胞术和DNA凝胶电泳检测骨髓细胞凋亡、免疫组化染色检测IL?11受体α及gp130的表达。结果表明,照射前应用IL?11对4.0Gy中子,照射后小鼠外周血白细胞和血小板降低有一定抑制作用,而照射后应用IL?11则对白细胞、红细胞、血小板以及骨髓有核细胞降低均有一定抑制作用;照射前及照射后用药组对细胞凋亡未见明显影响,而与单纯对照组比较,用药组、AgNOR含量增多,IL?11Rα及gp130表达均明显增强。说明IL?11可能通过受体α及gp130信号通路,促进损伤后造血功能恢复,从而发挥其对骨髓辐射损伤的防治作用。
To investigate the preventive and therapeutic effects of recombinant human interleukin 11 (rhIL-11) on the bone marrow injury in mice induced by lethal neutrons and its mechanism. Ninety-two male BALB / c mice were injected subcutaneously with rhIL? 11 three days before or after the 4.0Gy neutron whole body irradiation, and then killed and harvested at 6h, 1d and 2d after irradiation. The peripheral blood and bone marrow nuclei were counted cell. The content of nuclear argyrophilic protein in bone marrow was detected by Argyrophilic of Nucleolar Organorganisms (AgNOR) staining. The apoptosis of bone marrow cells was detected by flow cytometry and DNA gel electrophoresis. The levels of IL-11Rα and gp130 expression. The results showed that pretreatment with IL? 11 on 4.0Gy neutrons, irradiation, mice peripheral blood leukocytes and thrombocytopenia decreased a certain extent, while the application of IL? 11 irradiation on leukocytes, erythrocytes, platelets and bone marrow nucleated cells decreased But not before and after irradiation. However, compared with the control group, the content of AgNOR increased and the expression of IL-11Rα and gp130 increased obviously. IL? 11 may be through the receptor alpha and gp130 signaling pathway to promote hematopoietic recovery after injury, and thus play its role in the prevention and treatment of bone marrow radiation injury.