Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway
Unfractionated Heparin Ameliorates Lipopolysaccharide-Induced Lung Inflammation by Downregulating Nuclear Factor-κB Signaling Pathway
复制标题
普通肝素通过下调核因子-κB 信号通路改善脂多糖诱导的肺部炎症
DOI：
10.1007/s10753-013-9656-5
复制
发表时间：
2013-12-01
期刊：
影响因子：
5.1
通讯作者：
Ma, Xiaochun
中科院分区：
文献类型：
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作者：
Li, Xu;Li, ZhiLiang;Ma, Xiaochun
本研究旨在探讨普通肝素对脂多糖（LPS）诱导的大鼠内毒素血症和肺损伤的保护作用及其机制。以6 mg/kg静脉注射LPS。我们研究了普通肝素（100或300 U/kg）对LPS诱导的内毒素血症的治疗作用，通过静脉给药后，LPS的挑战。以湿/干重比值评价动物肺水肿程度。采用酶联免疫吸附试验和实时荧光定量RT-PCR法检测血清中白细胞介素-1 β（IL-1 β）和白细胞介素-6（IL-6）水平。Western blotting检测核因子-κ B（NF-κ B）的活化情况。研究表明，普通肝素治疗可减轻LPS诱导的急性肺损伤大鼠模型的炎症反应，且300 U/kg组效果更好。普通肝素发挥抗炎作用的机制与通过NF-κ B失活抑制IL-1 β和IL-6产生相关。
The present study aimed to determine the protective effects and the underlying mechanisms of unfractionated heparin on lipopolysaccharide (LPS)-induced endotoxemia and lung injury in rats. Rats were injected intravenously with LPS at 6 mg/kg. We examined the therapeutic effects of unfractionated heparin (100 or 300 U/kg) on LPS-induced endotoxemia by dosing intravenously simultaneously after LPS challenge. The animal lung edema degree was evaluated by wet/dry weight ratio. The levels of inflammatory mediators including interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) were assayed by enzyme-linked immunosorbent assay and quantitative real-time RT-PCR. The activation of nuclear factor-kappa B (NF-kappa B) was evaluated by Western blotting. The investigations revealed that treatment with unfractionated heparin can attenuate inflammatory responses in a rat model of LPS-induced acute lung injury, and the effect was much better in 300 U/kg group. The mechanisms by which unfractionated heparin exerts its anti-inflammatory effect are correlated with inhibition of IL-1 beta and IL-6 production via inactivation of NF-kappa B.