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肝素寡糖对脂多糖诱导人脐静脉内皮细胞炎症的影响及分子机制研究

Effect of heparin-derived oligosaccharide on lipopolysaccharides-induced inflammation in HUVECs and its molecular mechanisms

  • 摘要: 以脂多糖(LPS)诱导人脐静脉内皮细胞HUVECs炎症损伤,探讨肝素寡糖对炎症的影响及其分子机制。实验分为空白组(0.5%血清培养基)、模型组(LPS+0.5%血清培养基)及给药组(LPS+0.5%血清培养基+0.01、0.1、1 μmol/L HDO),采用活性氧实验检测细胞内活性氧簇水平,Western blot检测VCAM-1、p38、p-p38及核转录因子NF-κB等关键蛋白的表达水平。结果显示0.01、0.1和1 μmol/L的HDO可抑制100 μg/mL LPS诱导的HUVECs炎症因子VCAM-1表达水平,较弱的影响细胞中NF-κB分布,并下调信号通路中关键蛋白p38和p-p38表达。结果表明,HDO可能通过抑制炎症信号通路中关键蛋白的表达水平来抑制炎症因子的表达,从而起到抗炎作用。

     

    Abstract: In this study, the effect of heparin-derived oligosaccharide(HDO)on lipopolysaccharides(LPS)-induced inflammation in human umbilical vein endothelial cells(HUVECs)and the molecular mechanisms were investigated. The generation of intracellular reactive oxygen species(ROS)was detected by 20, 70-dichlorofluorescein diacetate(DCFH-DA). Experiment is divided into blank group(0. 5% serum medium), model group(LPS+0. 5% serum medium)and HDO dosing group(LPS+0. 5% serum medium +0. 01, 0. 1, 1mol/L HDO). The intracellular reactive oxygen species level was detected by reactive oxygen species experiment, the level of key regulatory proteins p38 and p-p38 in MAPK pathways and VCAM-1 were determined by Western blot. The results showed that HDO at 0. 01, 0. 1 and 1 μmol/L could inhibit the expression of VCAM-1 in HUVECs induced by 100 μg/mL LPS, and reduce the expression of key regulatory proteins p38 and p-p38, but could not obviously affect NF-κB nuclear translocation. The results all above showed that HDO could decrease the key regulatory proteins expression, and suppress the transcription of VCAM-1, resulting in inhibiting inflammation.

     

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