CAJ | 학술논문

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.
목적 관찰해수흡입형폐손상대서폐조직중적혈관긴장소Ⅱ(angiotensinⅡ,AngⅡ)급기수체혈관긴장소Ⅱ1형수체(angiotensinⅡtype 1 receptor,AT1)적변화정황,이급핵인자κB(NF-κB)신호전도통로재해수흡입형폐손상중적작용급기궤제.방법 40지SD대서수궤분위정상조、해수처리3h조、해수처리6h조화해수처리12 h조,매조10지,채용기관내적주해수(3 ml/kg)적방법제조해수흡입형폐손상모형.분별용방사면역분석방법화ELISA법검측폐조직중AngⅡ、종류배사인자α(tumor necrosis factor-α,TNF-α)화IL-1β적함량,병차용RT-PCR화Western blot방법검측폐조직중AT1화NF-κB적표체정황.결과 폐조직병리검사결과현시,불동시간적해수처리후가조성엄중적폐손상,기중해수처리6h후대서폐부손상최엄중.해수처리후AngⅡ적함량화AT1적표체명현승고;NF-κB재정상조표체흔소,해수처리후명현승고.여차동시,IL-1β화TNF-α재해수처리3h후함량신속증가,재해수처리6h후체고봉.결론 해수흡입가인기급성폐손상,AngⅡ통과격활AT1화NF-κB인기염증반응삼여해수흡입형폐손상적발생발전.
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.