期刊文献+

IL-1ra对FnLPS诱导人牙髓细胞合成IL-1β的拮抗作用

Interleukin-1 receptor antagonist reduces LPS stimulated IL-1β synthesis in human dental pulp cells.
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摘要 目的 :观察人重组白细胞介素 1受体拮抗剂 (IL - 1ra)对内毒素脂多糖 (LPS)刺激的人牙髓细胞分泌IL - 1β的拮抗作用。方法 :用ELISA夹心法检测IL - 1β含量。结果 :人牙髓细胞经LPS刺激后 ,IL - 1β含量明显增加。当加入高浓度的IL - 1ra后 ,IL - 1β含量与对照组相比有显著性降低 ,在LPS刺激牙髓细胞 6 0分钟以前加入一定浓度的IL - 1ra ,牙髓细胞培养上清液中IL - 1β的含量显著降低 ,但在 90分钟以后再加入IL - 1ra ,则IL - 1β的含量无明显变化。结论 :高剂量的IL - 1ra能够抑制LPS刺激的牙髓细胞分泌IL - 1β ,从而拮抗IL - 1的生物学活性。 Objective: This study was conducted to investigate that the effect of different concentrations of interleukin-1 receptor antagonist(IL-1ra) on the LPS induced IL-1β synthesis in human dental pulp cells. Methods: Measurement of IL-1β by sandwich ELISA. Results: The addition of LPS to the dental pulp cells significantly increased IL-1β production; The addition of certain concentrations of IL-1ra reduced LPS induced IL-1β synthesis in human pulp cells; Significant inhibition of the LPS induced IL-1β synthesis was observed when IL-1ra was added before treating with LPS for 60 min, while there is no effect after treating with LPS for 90 min. Conclusions: Certain of concentrations of IL-1ra can reduce LPS stimulated IL-1β synthesis.
出处 《口腔医学纵横》 CSCD 2000年第3期177-179,共3页 Journal of Comprehensive Stomatology
基金 国家自然科学基金资助项目!(批准号 :3 9470 75 2 )
关键词 内毒素脂多糖 人牙髓细胞 IL-1Β IL-1RA IL-1 Interleukin-1 receptor antagonist(IL-1ra) Interleukin-1β(IL-1β) Lipopolysaccharide(LPS) Human Dental pulp cells(HDP)
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参考文献4

  • 1D’souza R,Brown LR,Newland HR,et al.Detection and characterization of interleukin- 1 in human dental pulps[].Archives of Oral Biology.1989
  • 2Dinarello CA.Modalities for reducing interleukin-1 activity in disease[].Immunology Today.1993
  • 3Raetz CRH,Ulevitch RJ,Wright SD,et al.Gram negative endotoxin:an extraordinary lipid with profound effects on eukaryotic signal transduction[].The FASEB Journal.1991
  • 4Shanley TP,Peters JL,Jones ML et al.Regulatory effects of endogenous interleukin-1 receptor antagonist protein in immunoglobulin G immune complex - induced lung injury[].The Journal of Clinical Investigation.1996

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