超短波对大鼠急性肺损伤炎症反应的影响

Effects of ultrashort wave on inflammatory response in rats with acute lung injury

背景:超短波常用于肺部感染的对症治疗,有一定抗炎作用。炎症反应失控是急性肺损伤的重要发病机制,抑制炎症反应是控制急性肺损伤的重要策略。目的:观察超短波对大鼠急性肺损伤炎症反应的影响及炎症因子肿瘤坏死因子α、白细胞介素1β表达的影响。方法:24只3月龄雄性SD大鼠随机分为对照组、急性肺损伤组、超短波组,每组8只。急性肺损伤组与超短波组大鼠通过气管内滴注脂多糖复制急性肺损伤模型,对照组大鼠气管内滴注等量生理盐水。超短波组在大鼠滴注脂多糖即刻及滴注后4,8 h给予超短波干预,每次15 min。24 h后取材,对大鼠肺组织进行苏木精-伊红染色,肺组织病理学半定量评分和肺组织湿/干质量比值比较;ELISA检测血清炎症因子肿瘤坏死因子α、白细胞介素1β水平,RT-PCR、Western-blot分别检测肿瘤坏死因子α、白细胞介素1β的mRNA和蛋白表达水平。实验方案经南华大学附属第一医院医学伦理委员会批准(批准号为202002100009)。结果与结论:①肺组织湿/干质量比:急性肺损伤组较对照组明显升高(P<0.01),超短波组比急性肺损伤组降低,但差异无显著性意义;②病理表现:急性肺损伤组大鼠肺组织结构破坏明显、肺泡隔大小不一,肺泡壁不完整、变厚断裂,肺间质可见大量中性粒细胞浸润和部分红细胞渗出;超短波组肺泡结构相对完整清晰,肺间质炎症细胞浸润及红细胞渗出减少;③肺组织病理学半定量评分:急性肺损伤组较对照组明显升高(P<0.01);超短波组较急性肺损伤组明显降低(P<0.01);④急性肺损伤组的血清肿瘤坏死因子α、白细胞介素1β较对照组明显升高(均P<0.01),超短波组较急性肺损伤组明显降低(均P<0.05);⑤超短波组肺组织肿瘤坏死因子α、白细胞介素1βmRNA和蛋白较急性肺损伤组明显降低(均P<0.01或P<0.05);⑥结果说明,超短波可能通过下调炎症因子肿瘤坏死因子α、白细胞介素1β的表达,抑制急性肺损伤大鼠肺组织的炎症反应。

BACKGROUND:Ultrashort wave can inhibit the inflammatory response and is often used in symptomatic treatment of pulmonary infection.Uncontrolled inflammatory response is an important pathogenesis of acute lung injury.Inhibiting inflammation is an important strategy for controlling acute lung injury.OBJECTIVE:To observe the effects of ultrashort wave on inflammatory response and the expression of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)in rats with acute lung injury.METHODS:Twenty-four 3-month-old male Sprague-Dawley rats were randomly divided into control group,acute lung injury group(model group)and ultrashort wave group(n=8 per group).Rats in the acute lung injury group and the ultrashort wave group were given intratracheal lipopolysaccharide to replicate the acute lung injury model.Rats in the control group were given intratracheal infusion of the same amount of normal saline.In the ultrashort wave group,rats were given ultrashort wave intervention immediately,4 and 8 hours after lipopolysaccharide infusion,once for 15 minutes.Experimental animals were sacrificed 24 hours after intratracheal infusion of lipopolysaccharide or normal saline.The lung tissues of rats were compared by hematoxylin-eosin staining,lung histopathological semi-quantitative score and lung wet/dry weight ratio(W/D).Serum levels of inflammatory factors TNF-αand IL-1βwere detected by ELISA,and mRNA and protein expressions of TNF-αand IL-1βwere detected by RT-PCR and western blot,respectively.The study protocol was approved by the First Affiliated Hospital of Nanhua University,approved No.202002100009.RESULTS AND CONCLUSION:Lung W/D ratio in the acute lung injury group was significantly higher than that in the control group(P<0.01),whereas the ratio in the ultrashort wave group was lower than that in the acute lung injury group,but there was no significant difference between the two groups.Pathological manifestations:In the model group,the lung tissue structure was obviously damaged,with different sizes of alveolar septa,the alveolar wall was incomplete,thickened and fractured,a large number of neutrophils were seen in the lung interstitium,and some red blood cells were exudated.In the ultrashort wave group,compared with the model group,the alveolar structure was relatively complete and clear,and the infiltration of inflammatory cells and red blood cell exudation from the lung interstitium were reduced.Semi-quantitative histopathological score of the lung was significantly higher in the model group than the control group(P<0.01),but significantly reduced in the ultrashort wave group compared with the model group(P<0.01).Serum TNF-αand IL-1βlevels in the model group were significantly higher than those in the control group(both P<0.01).After ultrashort wave exposure,the levels of serum TNF-αand IL-1βsignificantly decreased compared to the model group(both P<0.05).After ultrashort wave exposure,the mRNA and protein expressions of TNF-αand IL-1βsignificantly decreased compared to the model group(P<0.01 or P<0.05).To conclude,ultrashort wave may inhibit the inflammatory response of the lung tissue in rats with acute lung injury by down-regulating the expression of inflammatory cytokines,TNF-αand IL-1β.