Zhang Yan, Li Hao, Yin Dan, Wu Mandi, Cui Yinghui, Wang Jinhuo, Cheng Zhanyu, Wang Yujia, Wang Huan, Guo Jianrong
Postgraduate Training Base at Shanghai Gongli Hospital, Ningxia Medical University, Shanghai, 200135, China.
Department of Anesthesiology, Gongli Hospital of Shanghai Pudong New Area, No. 219, Miaopu Road, Pudong New Area, Shanghai, 200135, People's Republic of China.
Clin Exp Med. 2025 May 22;25(1):171. doi: 10.1007/s10238-025-01703-1.
Elderly patients with lung dysfunction (EPLD) often experience chronic inflammation and impaired immune responses, significantly impacting their health outcomes. Currently, no specific treatment exists to prevent lung dysfunction in elderly patients. The detailed mechanism of lung dysfunction in elderly patients remains elusive, and this study aims to clarify it. General data and blood specimens were obtained from EPLD. A lung dysfunction mouse model was established by anesthetizing and ventilating BALB/c mice at a high tidal volume of 30 mL/kg. Blood samples and lung tissues were collected from all groups for further testing. HE staining, immunofluorescence, Western blot, ELISA, flow cytometry, and qRT-PCR were used to elucidate the molecular mechanisms of multidimensional integrated lung protection measures (MILPM) in lung dysfunction mice by targeting the NF-κB pathway. The results indicated that upregulation of the NF-κB signaling pathway accelerates the lung dysfunction process, while downregulation of the NF-κB signaling pathway can prevent it. Similarly, the upregulation of TNF-α, IL-6, IL-1β, and ROS levels is associated with the lung dysfunction process, whereas reducing their levels can serve as a preventative method against lung dysfunction development. Upregulation of the NF-κB pathway can accelerate the process of lung dysfunction.
老年肺功能障碍患者(EPLD)常经历慢性炎症和免疫反应受损,这对他们的健康结局有显著影响。目前,尚无预防老年患者肺功能障碍的特异性治疗方法。老年患者肺功能障碍的详细机制仍不清楚,本研究旨在阐明这一机制。从EPLD患者获取一般资料和血液标本。通过以30 mL/kg的高潮气量对BALB/c小鼠进行麻醉和通气建立肺功能障碍小鼠模型。从所有组收集血液样本和肺组织用于进一步检测。采用苏木精-伊红染色、免疫荧光、蛋白质免疫印迹、酶联免疫吸附测定、流式细胞术和定量逆转录聚合酶链反应,通过靶向核因子-κB(NF-κB)途径阐明肺功能障碍小鼠多维综合肺保护措施(MILPM)的分子机制。结果表明,NF-κB信号通路的上调加速了肺功能障碍进程,而NF-κB信号通路的下调可预防该进程。同样,肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)和活性氧(ROS)水平的上调与肺功能障碍进程相关,而降低它们的水平可作为预防肺功能障碍发展的方法。NF-κB途径的上调可加速肺功能障碍进程。