摘要
目的 观察海水吸入型肺损伤大鼠肺组织中的血管紧张素Ⅱ（angiotensinⅡ,AngⅡ）及其受体血管紧张素Ⅱ1型受体（angiotensinⅡtype 1 receptor,AT1）的变化情况,以及核因子κB（NF-κB）信号传导通路在海水吸入型肺损伤中的作用及其机制.方法 40只SD大鼠随机分为正常组、海水处理3h组、海水处理6h组和海水处理12 h组,每组10只,采用气管内滴注海水（3 ml/kg）的方法制造海水吸入型肺损伤模型.分别用放射免疫分析方法和ELISA法检测肺组织中AngⅡ、肿瘤坏死因子α（tumor necrosis factor-α,TNF-α）和IL-1β的含量,并且用RT-PCR和Western blot方法检测肺组织中AT1和NF-κB的表达情况.结果 肺组织病理检查结果显示,不同时间的海水处理后可造成严重的肺损伤,其中海水处理6h后大鼠肺部损伤最严重.海水处理后AngⅡ的含量和AT1的表达明显升高;NF-κB在正常组表达很少,海水处理后明显升高.与此同时,IL-1β和TNF-α在海水处理3h后含量迅速增加,在海水处理6h后达高峰.结论 海水吸入可引起急性肺损伤,AngⅡ通过激活AT1和NF-κB引起炎症反应参与海水吸入型肺损伤的发生发展.
Objective To observe the changes of angiotension Ⅱ （Ang Ⅱ） and angiotensin Ⅱ type 1 receptor （AT1） in seawater inhalation induced acute lung injury,as well as the role of nuclear factor-κB （NF-κB） pathway.Methods 40 Sprague Dawley rats were randomly divided into control group,seawater exposure 3 h group,seawater exposure 6 h group,and seawater exposure 12 h group.The lung injury model was established by endotracheal instillation of seawater （3 ml/kg）.Subsquently,the expression of Ang Ⅱ was measured by radioimmunoassay,interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） by ELISA,AT1 and NF-κB by RT-PCR and Western blot.Results The lung pathology results showed that seawater aspiration might result in lung injury especially 6 h after intratracheal instillation of seawater.The expressions of Ang Ⅱ and AT1 were significantly up-regulated in the seawater inhalation induced acute lung injury groups compared to the control group,so was the change of NFκB.The levels of IL-1β and TNF-α increased rapidly at 3 h after seawater aspiration and peaked at 6 h.Conclusions Seawater aspiration can cause acute lung injury by up-regulating the AT1 and NF-κB induced inflammatory response,in which Ang Ⅱ may play a crucial role.
出处
《国际呼吸杂志》
2014年第10期736-740,共5页
International Journal of Respiration
基金
国家自然科学基金（81270124）
