文章摘要
钱如云,刘嘉茵.TNF-α及sTNFRⅠ对子宫内膜异位症在位内膜基质细胞的作用[J].南京医科大学学报,2008,28(5):635~639
TNF-α及sTNFRⅠ对子宫内膜异位症在位内膜基质细胞的作用
The effects of TNF-α and sTNFRⅠ on stormal cells of endometriosis
投稿时间:2007-12-24  
DOI:10.7655
中文关键词: 子宫内膜异位症  基质细胞  TNF-α  IL-6  MMP-3
英文关键词: endometriosis  stroma cells  TNF-α  IL-6  MMP-3
基金项目:
作者单位
钱如云 南京医科大学第一附属医院妇产科,江苏 南京 210029 
刘嘉茵  
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中文摘要:
      目的:探讨肿瘤坏死因子α(tumor necrosis factor,TNF-α) 和可溶性肿瘤坏死因子受体(soluble TNFR I,sTNFR I)对体外培养的子宫内膜异位症(Endometriosis)患者在位内膜基质细胞的影响,为子宫内膜异位症的生物学治疗提供新思路?方法:对EMS 患者的在位子宫内膜基质细胞进行体外培养,分别用不同浓度的TNF-α(0?0.1?1.0?10.0和100.0 ng/ml)或者同一浓度TNF-α(1 ng/ml)培养不同时间(4?8?12?24?48和72 h)或者TNF-α(1 ng/ml)和sTNFRⅠ(2 ?滋g/ml)对基质细胞进行刺激并收集细胞上清液,利用双抗体夹心ELISA 检测细胞培养上清液中IL-6?基质金属蛋白酶-3(matrix metalloproteinases,MMP-3)的水平?结果:TNF-α可促进体外培养的EMS 子宫内膜基质细胞IL-6?MMP-3的分泌,而且IL-6 ?MMP-3浓度与TNF-α之间存在剂量?时间依赖关系(P < 0.05),而sTNFRⅠ具有抑制TNF-α的作用?结论:TNF-α在EMS的发病机制中发挥重要的作用,其对EMS 患者子宫内膜基质细胞的促黏附?侵袭?增殖等作用可能是通过促进IL-6?MMP-3 的分泌来完成的;sTNFRⅠ有望用于EMS生物学治疗?
英文摘要:
      Objective:To explore the effects of TNF-α and sTNFRⅠ on cultured eutopic endometrial stroma cells from endometriosis patients and find new biological therapy to endometriosis. Methods:Stroma cells from eutopic endometrium were cultured in vitro. TNF-α(0,0.1,1,10,and 100 ng/ml) was added to the medium in dose-responds experiment. TNF-alpha(1 ng/ml) was added for 0,4,8,12,24,48 and 72 hours in time-course experiment. TNF-α(0.1,1 and 10 ng/ml) and sTNFRⅠ(2 μg/ml) were added for 12 hours. Then the supernatant were collected to evaluate the productions of IL-6 and MMP-3. Results:The productions of IL-6 and MMP-3 in the supernatant of stroma cells from endometriosis were promoted by TNF-alpha in a dose-dependent and time-dependent manner. The productions of IL-6 and MMP-3 in the supernatant of stroma cells from endometriosis were promoted by TNF-alpha were decreased by sTNFRⅠ. Conclusion:TNF-α may promote the attachment and invade of stroma cells from women with endometriosis though inducing the expression of IL-6 and MMP-3 and play a central role in the pathogenesis of endometriosis. sTNFRⅠ may be the potential target for biological therapy to endometriosis.
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