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探索酸性物质吸入性肺损伤的机制。120只C57BL/6J小鼠随机分为稀盐酸(HCl)吸入组和生理盐水(NS)吸入组。实验小鼠经导管滴注0.1mol/L HCl/NS(1μl/g体重)至左肺,吸入后30min、2h、6h和24h分别检测小鼠的呼吸功能(Penh)(除外30min、肺湿干重比值(W/D)、支气管肺泡灌洗液(BALF)的白细胞计数和蛋白浓度,观察肺组织病理学改变;免疫组化研究小鼠左肺炎性细胞浸润变化;免疫印迹检测小鼠左肺肺组织炎性因子水平。12hHCl组的呼吸功能(Pehn)严重受损(P<0.01vs NS组),肺W/D明显高于其它时间组(P<0.05)和对照组(P<0.01vs NS组);BALF蛋白含量和白细胞总数在6hHCl组达到峰值(P<0.05vs其它时间组,P<0.01vs NS组);炎性因子IL-1β、TNF-α、NF-κB和IL-6在左肺组织中表达随HCl刺激时间逐渐升高,12h后表达量降低,24h时继续下降;HCl刺激30min即出现嗜中性粒细胞肺组织浸润,而巨噬细胞和T淋巴细胞出现相对较晚。研究通过吸入稀盐酸模拟吸入性肺炎小鼠模型,发现吸入性肺炎早期即有大量炎性因子,随后出现白细胞升高而巨噬细胞增多出现较晚;大量炎性因子均参与了整个疾病发生发展过程。另外,实验经气管单侧滴注法获得单侧吸入性肺炎的模型,更符合临床吸入性肺炎的特点,为临床深入研究吸入性肺炎制作了很好的动物模型。
Exploration of mechanism of acid inhalational lung injury. 120 C57BL / 6J mice were randomly divided into inhaled HCl (HCl) group and saline (NS) inhaled group. The mice were intratracheally instilled with 0.1mol / L HCl / NS (1μl / g body weight) into the left lung, and the respiratory function (Penh) was detected at 30min, 2h, 6h and 24h after inhalation (W / D), white blood cell count and protein concentration of bronchoalveolar lavage fluid (BALF) were measured. The pathological changes of lung tissue were observed. Immunohistochemical staining was used to study the changes of left lung inflammatory cell infiltration in mice. Western blotting was used to detect the left lung (P <0.01vs NS group), lung W / D was significantly higher than other time groups (P <0.05) and the control group (P <0.01vs) NS group). The protein content of BALF and the total number of leukocytes peaked in 6hHCl group (P <0.05vs for other time groups, P <0.01vs NS group); the inflammatory factors IL-1β, TNF-α, NF-κB and IL- In the left lung tissue, the expression of HCT increased gradually with the time of HCl stimulation, and the expression decreased after 12 hours and continued to decrease at 24h. The neutrophil lung tissue infiltration was observed after stimulated with HCl for 30 minutes, while the macrophages and T lymphocytes appeared relatively Night.Study inhalation of dilute hydrochloric acid in mice model of simulated aspiration pneumonia and found that there are a large number of early inflammatory pneumonia, inflammatory factors, followed by leukopenia While macrophages increased late; a large number of inflammatory factors are involved in the development of the entire disease process.In addition, the experiment by unilateral tracheal unilateral aspiration pneumonia model obtained more in line with the characteristics of clinical aspiration pneumonia, For the clinical in-depth study of aspiration pneumonia produced a good animal model.