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泮托拉唑通过一氧化氮通路促进 BMSCs 增殖及向成骨细胞定向分化 |
Pantoprazole promotes BMSCs proliferation and osteoblastic differentiation via NO pathway |
投稿时间:2013-05-05 |
DOI: |
中文关键词: 泮托拉唑 骨髓间质干细胞 一氧化氮 |
英文关键词:Pantoprazole Bone marrow-derived mesenchymal stem cells Nitric oxide |
基金项目:湖南省人民医院仁术基金资助项目(2010-50) |
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中文摘要: |
目的:探讨质子泵抑制剂泮托拉唑( Pantoprazole )对原代大鼠骨髓间质干细胞( Bone Marrow-derived Mesenchymal Stem Cells, BMSCs)的增殖及向成骨细胞分化的影响机制。方法建立原代大鼠BMSCs体外模型,在无酚红α-MEM培养基(含10%经葡聚糖包被炭末吸附的血清)中加入10 mmol/Lβ-甘油磷酸、50 mg/L维生素C和10 nmol/L地塞米松,诱导BMSCs向成骨细胞分化。给予不同浓度的泮托拉唑观察其对BMSCs的作用:观测MTT掺入率反映细胞增殖的情况;测定细胞内碱性磷酸酶活性与钙沉积量反映BMSCs向成骨细胞分化的状况;用一氧化氮试剂( Nitric oxide,NO)盒检测一氧化氮释放量。结果泮托拉唑在一定浓度范围内(0.1~10μmol/L)呈剂量依赖性增加原代大鼠BMSCs的MTT掺入率、细胞碱性磷酸酶活性及钙沉积量,并可适度增加一氧化氮释放量。结论泮托拉唑在0.1~10μmol/L剂量范围可通过一氧化氮信号传导通路促进原代BMSCs的增殖及其向成骨细胞的分化。 |
英文摘要: |
Objective To investigate the effect of pantoprazole, a proton pump inhibitor, on the proliferation and osteoblastic differentiation of primary rat bone marrow-derived mesenchymal stem cells ( BMSCs ) , and to explore its possible mechanism. Methods Rat BMSCs were cultured in osteogenic differentiation medium, consisting of phenol red-free α-MEM plus 10% FBS (dextran-coated charcoal stripped, DCS) supplemented with 10 mmol/Lβ-glycerophosphate, 50mg/L ascorbic acid, and 10 nmol/L dexamethasone, in order to induce the osteoblastic differentiation of BMSCs.Then, different concentrations of pantoprazole (0.01-10 μmol/L) were additioned into the medium, and its effect on BMSCs was observed.The cell proliferation was measured by MTT incorporation.The osteoblastic differentiation of BMSCs was assessed by the detection of cellular alkaline phosphatase ( ALP) activity and calcium deposition.The output of nitric oxide ( NO) was detected using a NO kit.Results In a concentration range (0.1-10 μmol/L), pantoprazole increased MTT incorporation, ALP activity, and calcium deposition of BMSCs in a dose-dependent manner.The output of NO also increased moderately.Conclusion Pantoprazole, at the concentration of 0.1 -10μmol/L, can promote proliferation and osteoblastic differentiation of primary BMSCs via NO pathway. |
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