摘要
目的探讨雾化吸入高渗盐水对脓毒症大鼠肺损伤的保护作用及机制。方法取健康成年SD大鼠30只,随机分为假手术组、模型组、高渗盐雾化组,每组10只。假手术组切开腹腔后常规缝合;模型组采用盲肠结扎穿孔法制备;高渗盐雾化组在脓毒症肺损伤造模后2 h给予3%高渗盐水雾化吸入;干预24 h后处死所有大鼠。评估3组大鼠肺组织病理学改变、肺组织湿/干重量(W/D)、髓过氧化物酶(MPO)活性、高迁移率族蛋白B1(HMGB1)、Toll样受体4(TLR4)、核因子-κB(NF-κB)表达及血清肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、IL-1β水平。结果与假手术组比较,模型组肺组织病理学评分肺组织W/D比值、MPO活性、HMGB1、TLR4、NF-κB蛋白表达水平及血清中TNF-α、IL-6、IL-1β水平均显著升高(P<0.01,P<0.05)。与模型组相比,高渗盐雾化组肺组织病理学评分、肺组织W/D比值、MPO活性、HMGB1、TLR4、NF-κB蛋白表达水平及血清中TNF-α、IL-6、IL-1β水平均显著降低(P<0.05,P<0.01)。结论高渗盐水雾化吸入可减轻脓毒症大鼠的肺损伤,其保护机制可能是通过抑制HMGB1/TLR4/NF-κB途径实现。
Objective To explore the protective effect and mechanism of inhalation of nebulized hypertonic saline on lung injury in septic rats.Methods Thirty healthy adult SD rats were randomly assigned to sham operation group,model group,and nebulized hypertonic saline group,with 10 rats in each group.In the sham operation group,the abdominal cavity was cut and sutured routinely,the model group was established by cecal ligation and perforation,and the nebulized hypertonic saline group received inhalation of 3%nebulized hypertonic saline at 2 h after modeling.The rats in each group were sacrificed at 24 h after intervention.The pathological changes and wet/dry weight(W/D)ratio of lung tissue in the three groups,the activity of myeloperoxidase(MPO)and the expression levels of high-modality groupbox 1(HMGB1),Toll like receptor 4(TLR4)and nuclear factor kappa B(NF-κB),and the serum levels of TNF-α,IL-6 and IL-1βwere evaluated in the three groups.Results Compared with the sham operation group,pathological score of the lung,W/D ratio of lung tissue,MPO activity,HMGB1,TLR4,NF-κB protein expression levels and serum TNF-α,IL-6,IL-1βlevels were significantly increased in the model group(P<0.01,P<0.05).Compared with the model group,pathological score of the lung,W/D ratio of lung tissue,MPO activity,expression levels of HMGB1,TLR4,NF-κB protein and serum levels of TNF,IL-6 and IL-1βwere significantly decreased(P<0.05,P<0.01).Conclusion Hypertonic salt nebulization can alleviate lung injury in septic rats,and its protective mechanism may be achieved by inhibiting HMGB1/TLR4/NF-κB pathway.
作者
樊菲菲
谢建刚
赵丹珲
王倩梅
程云会
刘传明
FAN Fei-fei;XIE Jian-gang;ZHAO Dan-hui;WANG Qian-mei;CHENG Yun-hui;LIU Chuan-ming(Department of Emergency Medicine,the First Affiliated Hospital,Military Medical University of PLA Air Force,Xi'an 710032,China;Department of Pathology,the First Affiliated Hospital,Military Medical University of PLA Air Force,Xi'an 710032,China)
出处
《解放军医药杂志》
CAS
2020年第11期1-5,共5页
Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
基金
国家自然科学基金青年项目(81601671)。