Kim Cherry, Jeong Sang Hoon, Lee Hong, Nam Yoon Jeong, Lee Hyejin, Choi Jin Young, Lee Yu-Seon, Kim Jaeyoung, Park Yoon Hee, Lee Ju-Han
Department of Radiology, Ansan Hospital, Korea University College of Medicine, 123, Jeokgeum-ro, Danwon-gu, Ansan-si, Gyeonggi, 15355, South Korea.
Medical Science Research Center, Ansan Hospital, Korea University College of Medicine, 123, Jeokgeum-ro, Danwon-gu, Ansan-si, Gyeonggi, 15355, South Korea.
Heliyon. 2024 Jul 14;10(14):e34562. doi: 10.1016/j.heliyon.2024.e34562. eCollection 2024 Jul 30.
Our study was to explore the effects of subchronic particulate matter (PM) exposure on lung injury induced by polyhexamethylene guanidine phosphate (PHMG-p) in a rat model. Specifically, we investigated pulmonary inflammation, fibrosis, and tumor formation using chest computed tomography (CT), and histopathologic examination. PHMG-p was administered intratracheally to 20 male rats. After an initial week of PHMG-p treatment, the experimental group (PM group) received intratracheal administration of PM suspension, while the control group received normal saline. This regimen was continued for 10 weeks to induce subchronic PM exposure. Chest CT scans were conducted on all rats, followed by the extraction of both lungs for histopathological analysis. All CT images underwent comprehensive quantitative and qualitative analyses. Pulmonary inflammation was markedly intensified in rats subjected to subchronic PM exposure in the PM group compared to those in the control. Similarly, lung fibrosis was more severe in the PM group as observed on both chest CT and histopathologic examination. Quantitative chest CT analysis revealed that the mean lesion volume was significantly greater in the PM group than in the control group. Although the incidence of bronchiolo-alveolar hyperplasia was higher in the PM group compared to the control group, this difference was not statistically significant. In summary, subchronic PM exposure exacerbated pulmonary inflammation and fibrosis underlying lung injury induced by PHMG-p.
我们的研究旨在探讨在大鼠模型中,亚慢性暴露于颗粒物(PM)对聚六亚甲基胍磷酸盐(PHMG-p)诱导的肺损伤的影响。具体而言,我们使用胸部计算机断层扫描(CT)和组织病理学检查来研究肺部炎症、纤维化和肿瘤形成情况。对20只雄性大鼠进行气管内给予PHMG-p。在PHMG-p治疗的初始一周后,实验组(PM组)接受气管内给予PM悬浮液,而对照组接受生理盐水。该方案持续10周以诱导亚慢性PM暴露。对所有大鼠进行胸部CT扫描,随后取出双肺进行组织病理学分析。所有CT图像均进行了全面的定量和定性分析。与对照组相比,PM组中经历亚慢性PM暴露的大鼠肺部炎症明显加剧。同样,在胸部CT和组织病理学检查中均观察到PM组的肺纤维化更严重。胸部CT定量分析显示,PM组的平均病变体积明显大于对照组。虽然PM组的细支气管肺泡增生发生率高于对照组,但这种差异无统计学意义。总之,亚慢性PM暴露加剧了PHMG-p诱导的肺损伤所潜在的肺部炎症和纤维化。