论文部分内容阅读
目的:探讨地塞米松和TLR4在大鼠淡水淹溺型肺损伤中的作用。方法:72只大鼠随机分为对照组、淹溺组和地塞米松组,通过淡水气道内吸入方法建立大鼠淡水淹溺型急性肺损伤模型,观察各时间点血气分析,检测0.5、2.0、4.0和8.0 h血清TNF-α、IL-6的含量以及肺组织湿/干重比值(W/D值)、MPO和TLR4 mRNA相对含量。结果:大鼠淡水淹溺型急性肺损伤模型建立成功;与对照组比较,淹溺组PaO2灌入淡水后急剧下降,随后逐渐回升,但仍维持较低水平。血清炎症因子TNF-α、IL-6分别在0.5、2.0 h开始表达,肺组织W/D值、MPO和TLR4 mRNA含量分别在淹溺后0.5、2.0和8.0 h升高。地塞米松可抑制炎症因子和TLR4 mRNA表达,减轻肺损伤。结论:TLR4参与淡水淹溺型大鼠肺损伤,地塞米松通过抑制其表达可减轻肺损伤。
Objective: To investigate the role of dexamethasone and TLR4 in lung injury in freshwater drowning rats. Methods: Seventy-two rats were randomly divided into control group, drowning group and dexamethasone group. Rat models of acute lung injury induced by freshwater drowning were established by fresh air inhalation. Blood gas analysis was performed at each time point to detect 0.5,2.0 , 4.0 and 8.0 h serum TNF-α, IL-6 content and lung tissue wet / dry weight ratio (W / D value), MPO and TLR4 mRNA relative content. Results: The model of acute lung injury induced by freshwater drowning in rats was established successfully. Compared with the control group, PaO2 dropped sharply in freshwater drowning group, then rose gradually but remained at a low level. Serum inflammatory cytokines such as TNF-α and IL-6 began to express at 0.5 and 2.0 h, and W / D, MPO and TLR4 mRNA levels in lung tissue increased at 0.5, 2.0 and 8.0 h after flooding respectively. Dexamethasone can inhibit the expression of inflammatory cytokines and TLR4 mRNA and reduce lung injury. CONCLUSION: TLR4 is involved in lung injury in freshwater drowning rats. Dexamethasone can reduce lung injury by inhibiting its expression.