Lian Zhichuang, Kuerban Remila, Niu Zongxin, Aisaiti Paruzha, Wu Chao, Yang Xiaohong
Graduate School Xinjiang Medical University, Urumqi 830001, China.
Department of Respiratory and Critical Care Medicine People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China.
Emerg Med Int. 2024 Aug 6;2024:7610032. doi: 10.1155/2024/7610032. eCollection 2024.
This study explored the molecular mechanism underlying the association of Notch signaling and oxidative stress with the occurrence of pulmonary fibrosis in patients with pigeon breeder's lung (PBL). Rat models of fibrotic PBL were constructed with freeze-dried protein powder, and the animals were divided into the control (intratracheal instillation of normal saline; = 9), M (PBL model; intratracheal instillation of freeze-dried protein powder; = 9), and M + D (PBL+ the Notch inhibitor DAPT; = 9) groups. Immunohistochemistry was employed to observe the protein levels of pathway factors and -SMA, and the levels of ROS, GSH-PX, SOD, and MDA were observed using ELISA. To verify the results of the animal experiment, cytological models were constructed. The M group and the M + D group had significantly increased -SMA levels ( < 0.05). Although both groups had significantly higher key protein levels in the Notch channel, the M + D group had significantly lower levels relative to the M group ( < 0.05). Oxidative stress products were examined, and the levels of MDA and ROS were significantly increased, while those of GSH-PX and SOD were significantly decreased in the M and M + D groups as compared to the control, but the M group and the M + D group significantly differed ( < 0.05). These findings were further validated by the cytological experiment. Notch signaling is associated with pulmonary fibrosis in PBL by regulating cellular oxidative stress, and inhibiting this pathway can slow down pulmonary fibrosis progression.
本研究探讨了Notch信号通路和氧化应激与鸽饲养者肺（PBL）患者肺纤维化发生之间关联的分子机制。用冻干蛋白粉构建PBL纤维化大鼠模型，将动物分为对照组（气管内滴注生理盐水；n = 9）、M组（PBL模型组；气管内滴注冻干蛋白粉；n = 9）和M + D组（PBL + Notch抑制剂DAPT；n = 9）。采用免疫组织化学法观察通路因子和α - SMA的蛋白水平，用酶联免疫吸附测定法观察ROS、GSH - PX、SOD和MDA的水平。为验证动物实验结果，构建了细胞学模型。M组和M + D组的α - SMA水平显著升高（P < 0.05）。虽然两组Notch通道中的关键蛋白水平均显著升高，但M + D组相对于M组水平显著降低（P < 0.05）。检测氧化应激产物，与对照组相比，M组和M + D组的MDA和ROS水平显著升高，而GSH - PX和SOD水平显著降低，但M组和M + D组差异显著（P < 0.05）。细胞学实验进一步验证了这些结果。Notch信号通路通过调节细胞氧化应激与PBL中的肺纤维化相关，抑制该通路可减缓肺纤维化进程。
