Qin Mengting, Qiu Zhongpeng
Department of Critical Care Medicine, The First Affiliated Hospital of Medical College, Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
Department of Orthopedics, The First Affiliated Hospital of Medical College, Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
Exp Ther Med. 2019 Jan;17(1):383-387. doi: 10.3892/etm.2018.6926. Epub 2018 Nov 5.
Changes in tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and vascular endothelial growth factor (VEGF) in serum and bronchoalveolar lavage fluid (BALF) in rats with acute respiratory distress syndrome (ARDS) and the intervention effect of dexamethasone were observed to explore the theoretical basis of dexamethasone in the treatment of ARDS. Seventy-two rats were randomly divided into normal control group (group N, n=24), ARDS model group (group L, n=24) and dexamethasone group (group D, n=24). The ARDS rat model was established by jointly injecting oleic acid and lipopolysaccharide via the caudal vein, while rats in group D received intervention with dexamethasone. The wet/dry weight ratios of lung tissues were measured, and the levels of TNF-α, IL-6, IL-10 and VEGF in serum and BALF were measured via enzyme-linked immunosorbent assay. The wet/dry weight ratio of lung tissues of rats in group D was significantly decreased compared with that in group L (P<0.05 or P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group L and D were obviously increased compared with those in group N at each time point (P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group D were significantly decreased compared with those in group L (P<0.01). In conclusion, there is a serious imbalance between anti-inflammatory response and inflammatory response in rats with ARDS induced by oleic acid combined with lipopolysaccharide of , whereas dexamethasone can alleviate lung injury through inhibiting expression levels of inflammatory factors and promoting expression levels of anti-inflammatory factors.
观察急性呼吸窘迫综合征(ARDS)大鼠血清及支气管肺泡灌洗液(BALF)中肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、IL-10和血管内皮生长因子(VEGF)的变化以及地塞米松的干预作用,以探讨地塞米松治疗ARDS的理论依据。将72只大鼠随机分为正常对照组(N组,n = 24)、ARDS模型组(L组,n = 24)和地塞米松组(D组,n = 24)。通过尾静脉联合注射油酸和脂多糖建立ARDS大鼠模型,D组大鼠接受地塞米松干预。测定肺组织湿/干重比,采用酶联免疫吸附测定法检测血清及BALF中TNF-α、IL-6、IL-10和VEGF的水平。D组大鼠肺组织湿/干重比与L组相比显著降低(P<0.05或P<0.01)。各时间点L组和D组大鼠血清及BALF中TNF-α、IL-6和VEGF水平与N组相比明显升高(P<0.01)。D组大鼠血清及BALF中TNF-α、IL-6和VEGF水平与L组相比显著降低(P<0.01)。综上所述,油酸联合脂多糖诱导的ARDS大鼠抗炎反应与炎症反应严重失衡,而地塞米松可通过抑制炎症因子表达水平和促进抗炎因子表达水平来减轻肺损伤。