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目的探讨当归多糖(Angelica polysaccharide,APS)预防给药对放射损伤小鼠骨髓单个核细胞(Bone marrow mononuclear cells,BMNCs)黏附分子表达及细胞周期的影响。方法将BALB/c小鼠分为4组:正常对照组(不作任何处理)、NS组(经腹腔注射生理盐水)、2mg/kgAPS组(经腹腔注射2mg/kgAPS)和8mg/kgAPS组(经腹腔注射8mg/kgAPS),连续注射7d后,进行照射,并继续给药13d。分别于照射后第7、14天采集各组小鼠外周血,并取骨髓,进行WBC、RBC、PLT及BMNC计数;流式细胞术检测小鼠Sca-1+BMNC表面黏附分子CD44和CD49d的表达及BMNC细胞周期的变化;半定量RT-PCR和Western blot法分别检测小鼠BMNC细胞周期蛋白D(2CyclinD2)mRNA转录水平和蛋白表达水平的变化。结果与正常对照组比较,NS组外周血WBC、RBC、PLT及BMNC数量均明显减少,Sca-1+BMNC表面黏附分子CD44和CD49d的表达明显下降(P<0.05),G0/G1期细胞比例显著增加(P<0.05),CyclinD2 mRNA转录水平和蛋白表达水平均明显降低(P<0.05);2mg/kgAPS组和8mg/kgAPS组能增加外周血各指标及BMNC数量(P<0.05),明显降低第7和14天Sca-1+BMNC表面黏附分子CD44和CD49d的表达水平(P<0.05),降低G0/G1期细胞比例(P<0.05),提高CyclinD2 mRNA的转录水平和蛋白表达水平(P<0.05)。结论 APS预防给药能通过降低放射损伤小鼠Sca-1+BMNC表面黏附分子的表达水平,上调BMNC的CyclinD2 mRNA和蛋白表达来加速BMNCG1期向S期的转换,促进造血恢复。
Objective To investigate the effect of Angelica polysaccharide (APS) on adhesion molecule expression and cell cycle of Bone marrow mononuclear cells (BMNCs) in radiation-injured mice. Methods BALB / c mice were divided into 4 groups: normal control group (no treatment), NS group (intraperitoneal injection of normal saline), 2mg / kg APS group (intraperitoneal injection of 2mg / kg APS) and 8mg / kg APS group Intraperitoneal injection of 8mg / kgAPS), continuous injection of 7d, irradiation, and continue to administer 13d. Peripheral blood of mice in each group were collected on the 7th and 14th day after irradiation, and the bone marrow was taken for WBC, RBC, PLT and BMNC counting. Flow cytometry was used to detect the expression of CD44 and CD49d on the surface of Sca-1 + BMNC The expression of 2CyclinD2 mRNA and protein in BMNC of mice were detected by semi-quantitative RT-PCR and Western blot respectively. Results Compared with the normal control group, the numbers of WBC, RBC, PLT and BMNC in peripheral blood of NS group were significantly decreased, the expressions of CD44 and CD49d on the surface of Sca-1 + BMNC were significantly decreased (P <0.05) (P <0.05). Both 2mg / kg APS and 8mg / kg APS increased the number of peripheral blood and the number of BMNC (P <0.05), and significantly increased the expression of CyclinD2 mRNA and protein (P <0.05) Decreased the expression of CD44 and CD49d on the surface of Sca-1 + BMNC on day 7 and 14 (P <0.05), decreased the proportion of cells in G0 / G1 phase (P <0.05), and increased the transcriptional and protein expression of CyclinD2 P <0.05). Conclusion APS can accelerate the conversion of BMNCG1 to S phase and decrease hematopoietic recovery by decreasing the expression of adhesion molecules on Sca-1 + BMNC and increasing the expression of CyclinD2 mRNA and protein in BMNC of radiation-injured mice.