【摘要】：目的利用鹽酸誘導(dǎo)小鼠急性肺損傷模型,研究P-選擇素糖蛋白配體(PSGL-1)在其中的作用及可能機(jī)制。方法野生型小鼠(WT)和PSGL-1敲除小鼠(PSGL-1-/-)隨機(jī)分為生理鹽水組和鹽酸組,經(jīng)導(dǎo)管左肺滴注生理鹽水或0.1 mol/L鹽酸(1μl/g體重),2 h后測(cè)定小鼠肺功能指標(biāo)增強(qiáng)呼氣間歇(Penh)、PaO_2和PaCO_2、肺濕干重比值(W/D)以及支氣管肺泡灌洗液(BALF)總蛋白濃度和白細(xì)胞計(jì)數(shù)。鏡下觀察靶肺組織炎癥細(xì)胞浸潤(rùn)情況,并檢測(cè)肺組織炎癥因子IL-6和IL-1β及核因子-κB(NF-κB)p65、IκBa和p-IκBa蛋白表達(dá)水平。結(jié)果鹽酸刺激后,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]較WT組顯著降低(P0.05),而PaO_2較WT組顯著增高[(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蛋白濃度[(3.71±0.64)μg/μl vs.(4.74±0.98)μg/μl]及白細(xì)胞總數(shù)[(13.00±2.18)×10~7/L vs.(49.42±3.35)×10~7/L]較WT小鼠明顯降低(P0.05)。肺組織炎癥因子IL-6、IL-1β及p65和p-IκBa表達(dá)水平顯著低于WT組,而IκBa表達(dá)水平明顯高于WT組(P0.05)。與PSGL-1敲除小鼠比較,鹽酸誘導(dǎo)的WT小鼠肺組織出現(xiàn)了更為明顯的中性粒細(xì)胞和巨噬細(xì)胞浸潤(rùn)。生理鹽水誘導(dǎo)的對(duì)照組小鼠各項(xiàng)檢測(cè)指標(biāo)未出現(xiàn)顯著差異,但均明顯低于其相應(yīng)鹽酸組(IκBa除外,P0.05)。結(jié)論 PSGL-1可能通過(guò)激活NF-κB信號(hào)通路促進(jìn)肺組織白細(xì)胞的浸潤(rùn)及炎癥反應(yīng),在急性肺損傷疾病的發(fā)生發(fā)展中發(fā)揮重要的作用。
[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. 緇撴灉鐩愰吀鍒烘縺鍚，

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