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内吗啡肽-1对正常骨髓基质细胞造血调控的影响

发布时间:2018-07-25 19:53
【摘要】: 目的研究内吗啡肽-1对正常骨髓基质细胞表面细胞间黏附分子(intercellularadhesion molecule,ICAM-1)、血管细胞黏附分子(Vascular cell adhesion molecule,VCAM-1),和基质细胞分泌的细胞因子IL-6、TNF-a的调控作用。 方法Ficoll密度梯度离心法分离骨髓基质细胞,应用流式细胞术检测其表面标志。流式细胞术检测黏附分子ICAM-1和VCAM-1的表达,酶联免疫吸附法检测细胞因子IL-6、TNF-a的浓度。 结果黏附分子的表达:正常骨髓基质细胞加入内吗啡肽-1培养24h后各实验组ICAM-1和VCAM-1表达与对照组比较有显著性差异(P<0.05),而在相同内吗啡肽-1浓度下,培养时间的的变化对于二者的表达无明显影响;细胞因子的分泌水平:不管是量效关系还是时效关系,IL-6、TNF-a的浓度实验各组数据与对照组比较无显著性差异(P>0.05) 结论1内吗啡肽-1能调控正常骨髓基质表面ICAM-1和VCAM-1的表达。 2内吗啡肽-1对于正常骨髓基质细胞分泌的细胞因子IL-6、TNF-a无明显促进或抑制作用。
[Abstract]:Objective to investigate the effects of endomorphin 1 on intercellularadhesion molecule-1 (ICAM-1), (Vascular cell adhesion molecule-1 (VCAM-1) and the cytokine IL-6 / TNF-a secreted by stromal cells in normal bone marrow stromal cells. Methods Bone marrow stromal cells were isolated by Ficoll density gradient centrifugation and their surface markers were detected by flow cytometry. The expression of ICAM-1 and VCAM-1 was detected by flow cytometry and the concentration of cytokine IL-6 and TNF-a was detected by enzyme-linked immunosorbent assay (Elisa). Results the expression of adhesion molecules: the expression of ICAM-1 and VCAM-1 in normal bone marrow stromal cells cultured with endomorphin 1 for 24 hours was significantly different from that in control group (P < 0. 05), but at the same concentration of endomorphin 1, the expression of ICAM-1 and VCAM-1 in each experimental group was significantly higher than that in control group (P < 0. 05). The change of culture time had no significant effect on the expression of both. Levels of cytokines secretion: no significant difference was found in the concentration of IL-6 and TNF-a between the dose-response and time-dependent groups (P > 0.05). Conclusion 1 morphine peptide 1 can regulate the normal bone marrow base. The expression of ICAM-1 and VCAM-1 on the cytoplasm. 2 morphine peptide 1 had no obvious effect on the cytokine IL-6 and TNF-a secreted by normal bone marrow stromal cells.
【学位授予单位】:兰州大学
【学位级别】:硕士
【学位授予年份】:2009
【分类号】:R329

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