摘要
目的探索烟雾吸入损伤大鼠肺组织水通道蛋白(AQP)1、AQP5表达水平。方法将健康成年雄性SD大鼠随机分为对照组(NC组,6例)和烟雾吸入组(B组,40例)。B组大鼠烟雾吸入15 min,制备烟雾吸入损伤模型,分别于1、6、12和24 h(B1 h、B6 h、B12 h和B24 h)处理大鼠并采集标本,检测血浆炎症指标肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6),肺组织湿干比和肺组织病理染色,取肺组织检测AQP1和AQP5 mRNA和蛋白水平。结果烟雾吸入后,烟雾吸入组大鼠死亡11只,存活29只,存活率72.5%;烟雾吸入后1、6、12、24 h血浆炎症指标TNF-α、IL-6水平升高,肺组织湿干比值升高,与NC组比较,差异有统计学意义(P<0.05);病理显示烟雾吸入大鼠肺组织弥漫性损伤,可见不同程度炎症细胞浸润、出血水肿以及肺泡间隔增厚;烟雾吸入各组肺组织AQP1、AQP5 mRNA以及蛋白表达水平降低,与NC组比较差异有统计学意义(P<0.05),免疫组织化学显示AQP1、AQP5蛋白染色变浅。结论烟雾吸入可以导致大鼠急性肺损伤,肺组织水肿,肺组织AQP1、AQP5表达水平下降;AQP1、AQP5表达降低是烟雾吸入损伤时渗出水肿、组织损伤的致伤机制。
Objective To investigate the expression levels of aquaporin1(AQP1),AQP5 in rat lung tissues with smoke inhalation injury.Methods Healthy adult male Sprague-Dawley(SD)rats were randomly divided into a control group(NC group)(n=6)and a smoke inhalation group(B group)(n=40).Rats in the B group were exposed to smoke inhalation for 15 minutes to induce smoke inhalation injury.At 1,6,12,and 24 hours after exposure(B1 h,B6 h,B12 h,and B24 h),the rats were treated and specimens were collected.Plasma inflammatory markers TNF-αand IL-6,lung tissue wet-to-dry ratio,and lung tissue histopathological staining were measured.Lung tissue samples were collected to detect the mRNA and protein levels of AQP1 and AQP5.Results After smoke inhalation,11 rats in the smoke inhalation group died while 29 rats survived,resulting in a survival rate of 72.5%.The plasma levels of inflammatory markers TNF-αand IL-6,as well as the lung tissue wet-to-dry ratio,were significantly increased at 1,6,12,and 24 hours after smoke inhalation compared to NC group(P<0.05).Histopathological analysis revealed diffuse lung tissue injury in the smoke inhalation rats,characterized by varying degrees of inflammatory cell infiltration,hemorrhage,edema,and alveolar septal thickening.The mRNA and protein expression levels of AQP1 and AQP5 in the lung tissues of the smoke inhalation groups were significantly decreased compared to NC group(P<0.05).Immunohistochemistry staining showed lighter staining of AQP1 and AQP5 proteins in the lung tissues of rats after smoke inhalation.Conclusion Smoke inhalation can lead to acute lung injury in rats,characterized by lung tissue edema and decreased expression levels of AQP1 and AQP5.The decreased expression of AQP1 and AQP5 is a pathogenic mechanism for the development of exudative edema and tissue injury in smoke inhalation injury.
作者
李虎明
韩志海
张春阳
陈旭昕
张燕
陈韦
LI Huming;HAN Zhihai;ZHANG Chunyang;CHEN Xuxin;ZHANG Yan;CHEN Wei(Department of Pulmonary and Critical Care Medicine,The Sixth Medical Center of PLA General Hospital,Beijing 100048,China)
出处
《转化医学杂志》
2025年第5期110-115,共6页
Translational Medicine Journal
基金
北京市自然科学基金(7232169)。
关键词
烟雾吸入性急性肺损伤
肺水肿
水通道蛋白
大鼠
Smoke inhalation induced acute lung injury
Pulmonary edema
Aquaporins
Rat
作者简介
李虎明,硕士研究生,副主任医师。主要从事急性肺损伤与呼吸危重症方向研究;通信作者:韩志海,E-mail:hanzhihai@301hospital.com.cn。
