孙兰, 汪青, 刘景生. 雌激素促进人的类成骨细胞TE85成骨作用的受体机制J. 药学学报, 1999, 34(8): 561-564.
引用本文: 孙兰, 汪青, 刘景生. 雌激素促进人的类成骨细胞TE85成骨作用的受体机制J. 药学学报, 1999, 34(8): 561-564.
Sun Lan, Wang Qing, Liu Jingsheng, . RECEPTOR MECHANISM OF ESTROGEN STIMULATING BONE FORMATION IN HUMAN OSTEOBLAST-LIKE CELL LINE TE85J. Acta Pharmaceutica Sinica, 1999, 34(8): 561-564.
Citation: Sun Lan, Wang Qing, Liu Jingsheng, . RECEPTOR MECHANISM OF ESTROGEN STIMULATING BONE FORMATION IN HUMAN OSTEOBLAST-LIKE CELL LINE TE85J. Acta Pharmaceutica Sinica, 1999, 34(8): 561-564.

雌激素促进人的类成骨细胞TE85成骨作用的受体机制

RECEPTOR MECHANISM OF ESTROGEN STIMULATING BONE FORMATION IN HUMAN OSTEOBLAST-LIKE CELL LINE TE85

  • 摘要: 目的:研究雌激素促进人的类成骨细胞株TE85细胞骨形成的作用。方法:用3H-胸腺嘧啶、3H-脯氨酸参入法分别测定细胞的增殖和胶原合成; 紫外分光光度法测定细胞内骨碱性磷酸酶(ALP)活性; 放免法测定细胞内骨钙素(BGP)含量; 放射配基法测定细胞核雌激素受体结合。结果:雌激素(E2, 0.01~1.0 nmol.L-1)可浓度依赖地刺激TE85细胞的3H-胸腺嘧啶和3H-脯氨酸的参入量; 在相同的时间点和剂量下,可增加成骨细胞内ALP活性和BGP的含量。结论:E2通过增加成骨细胞数量、促进细胞胶原蛋白及ALP和BGP的合成而促进成骨作用,这些作用是通过雌激素受体介导的。

     

    Abstract: AIM: To study the effects of estrogen on stimulating bone formation in osteoblast-like cell line TE85. METHODS: Utilizing methods of 3H-thymidine incorporation for cell proliferation, 3H-proline incorporation for collagen synthesis, ultraviolet spectrophotometry for measurement of alkaline phosphatase (ALP) activity, radioimmunoassay for bone gla-protein (BGP) content assay, and radio-ligand binding for estrogen receptor assay. RESULTS: Cells were incubated with various concentrations (from 0.01 to 10 nmol.L-1) of 17β-estradiol (E2) for 48 h and 72 h, 3H-thymidine incorporation into DNA was increased gradually while 3H-proline incorporation was enhanced in the same fashion. E2 at the same dose increased the intracellular ALP activity and BGP content at the same time. In ligand-receptor binding experiment, the KD of 3H-E2 saturation test was 2.59×10-10 mol.L-1 in TE85 cells and the receptor number was found to be 262.7±64.6 site per cell. The IC50 of 4-OH-tamoxifen and ICI 182,780 were 0.99×10-8 mol.L-1 and 8×10-10 mol.L-1, respectively. CONCLUSION: E2 improved bone formation by ways of stimulating cell proliferation, enhancing collagen synthesis, ALP activity, and BGP content. The effects of E2 were performed by the mediation of estrogen receptor.

     

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