P-选择素糖蛋白配体在盐酸诱导小鼠急性肺损伤中的作用机制研究

发布时间：2018-09-04 06:59

【摘要】：目的利用盐酸诱导小鼠急性肺损伤模型,研究P-选择素糖蛋白配体(PSGL-1)在其中的作用及可能机制。方法野生型小鼠(WT)和PSGL-1敲除小鼠(PSGL-1-/-)随机分为生理盐水组和盐酸组,经导管左肺滴注生理盐水或0.1 mol/L盐酸(1μl/g体重),2 h后测定小鼠肺功能指标增强呼气间歇(Penh)、PaO_2和PaCO_2、肺湿干重比值(W/D)以及支气管肺泡灌洗液(BALF)总蛋白浓度和白细胞计数。镜下观察靶肺组织炎症细胞浸润情况,并检测肺组织炎症因子IL-6和IL-1β及核因子-κB(NF-κB)p65、IκBa和p-IκBa蛋白表达水平。结果盐酸刺激后,PSGL-1敲除小鼠Penh(4.77±1.22 vs.5.80±0.84)和PaCO_2[(63.7±3.9)mm Hg vs.(74.4±7.4)mm Hg]较WT组显著降低(P0.05),而PaO_2较WT组显著增高[(81.0±7.1)mm Hg vs.(62.0±8.9)mm Hg,P0.05],肺W/D(4.86±0.15 vs.5.22±0.20)和BALF蛋白浓度[(3.71±0.64)μg/μl vs.(4.74±0.98)μg/μl]及白细胞总数[(13.00±2.18)×10~7/L vs.(49.42±3.35)×10~7/L]较WT小鼠明显降低(P0.05)。肺组织炎症因子IL-6、IL-1β及p65和p-IκBa表达水平显著低于WT组,而IκBa表达水平明显高于WT组(P0.05)。与PSGL-1敲除小鼠比较,盐酸诱导的WT小鼠肺组织出现了更为明显的中性粒细胞和巨噬细胞浸润。生理盐水诱导的对照组小鼠各项检测指标未出现显著差异,但均明显低于其相应盐酸组(IκBa除外,P0.05)。结论 PSGL-1可能通过激活NF-κB信号通路促进肺组织白细胞的浸润及炎症反应,在急性肺损伤疾病的发生发展中发挥重要的作用。
[Abstract]:Objective to study the role and possible mechanism of P-selectin glycoprotein ligand (PSGL-1) in acute lung injury induced by hydrochloric acid in mice. Methods (WT) and PSGL-1 knockout mice (PSGL-1-/-) were randomly divided into saline group and hydrochloric acid group. The lung function indexes of mice were measured after intrapulmonary infusion of normal saline or 0.1 mol/L hydrochloric acid (1 渭 l / g BW) for 2 hours. The ratio of lung wet to dry weight (W / D), the total protein concentration of (BALF) in bronchoalveolar lavage fluid (BALF) and the white blood cell count (WBC) in the bronchoalveolar lavage fluid were measured. The infiltration of inflammatory cells in target lung tissue was observed under microscope, and the expression levels of inflammatory factors IL-6 and IL-1 尾, nuclear factor- 魏 B (NF- 魏 B) p65 I 魏 Ba and p-I 魏 Ba were detected. 缁撴灉鐩愰吀鍒烘縺鍚，

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