Abstract：
OBJECTIVE: To investigate the impact of maternal smoking on chronic obstructive pulmonary disease (COPD) progression in offspring.
METHODS: Using female C57BL/6 J mice, a maternal cigarette smoke exposure (CSE) model was established. Mice were exposed to cigarette smoke for 2 hours/day, 7 days/week, with a minimum 4-hour interval between exposures. Experimental groups included control (Con), pregnancy exposure (AS), pre-pregnancy exposure (SA), and pre-pregnancy + pregnancy exposure (SS). Lung function tests (Penh, PAU, TVb, EF50, Tr) were conducted on male offspring at 7 weeks. Histopathology, electron microscopy, and protein level changes were examined.
RESULTS: Lung function tests revealed significant impairments in Penh, PAU, TVb, EF50, and Tr in offspring across all exposure scenarios. Specifically, AS experienced significant lung function impairment and mitochondrial dysfunction in offspring, with noticeable pulmonary lesions and increased apoptosis. SA showed similar or even more severe lung function impairment and cellular apoptosis. SS exhibited the most pronounced effects, with the highest levels of lung dysfunction, mitochondrial damage, and apoptosis. Histopathological analysis showed pulmonary lesions in offspring exposed to maternal CSE. Flow cytometry revealed increased apoptosis and reduced mitochondrial membrane potential in offspring lung cells. Electron microscopy confirmed mitochondrial dysfunction. Upregulation of apoptotic proteins and downregulation of anti-apoptotic protein Bcl-2 were found in offspring lung tissue exposed to maternal CSE.
CONCLUSIONS: Maternal smoking induces impaired lung function, pulmonary lesions, and mitochondrial dysfunction in offspring, regardless of exposure timing and duration. Additionally, it alters expression of apoptosis-related proteins in offspring lung tissue, potentially contributing to COPD susceptibility.
METHODS: Using female C57BL/6 J mice, a maternal cigarette smoke exposure (CSE) model was established. Mice were exposed to cigarette smoke for 2 hours/day, 7 days/week, with a minimum 4-hour interval between exposures. Experimental groups included control (Con), pregnancy exposure (AS), pre-pregnancy exposure (SA), and pre-pregnancy + pregnancy exposure (SS). Lung function tests (Penh, PAU, TVb, EF50, Tr) were conducted on male offspring at 7 weeks. Histopathology, electron microscopy, and protein level changes were examined.
RESULTS: Lung function tests revealed significant impairments in Penh, PAU, TVb, EF50, and Tr in offspring across all exposure scenarios. Specifically, AS experienced significant lung function impairment and mitochondrial dysfunction in offspring, with noticeable pulmonary lesions and increased apoptosis. SA showed similar or even more severe lung function impairment and cellular apoptosis. SS exhibited the most pronounced effects, with the highest levels of lung dysfunction, mitochondrial damage, and apoptosis. Histopathological analysis showed pulmonary lesions in offspring exposed to maternal CSE. Flow cytometry revealed increased apoptosis and reduced mitochondrial membrane potential in offspring lung cells. Electron microscopy confirmed mitochondrial dysfunction. Upregulation of apoptotic proteins and downregulation of anti-apoptotic protein Bcl-2 were found in offspring lung tissue exposed to maternal CSE.
CONCLUSIONS: Maternal smoking induces impaired lung function, pulmonary lesions, and mitochondrial dysfunction in offspring, regardless of exposure timing and duration. Additionally, it alters expression of apoptosis-related proteins in offspring lung tissue, potentially contributing to COPD susceptibility.
摘要：
目的：探讨母亲吸烟对子代慢性阻塞性肺疾病(COPD)进展的影响。
方法：使用雌性C57BL/6J小鼠，建立母体香烟烟雾暴露(CSE)模型。小鼠暴露于香烟烟雾2小时/天，7天/周,曝光之间至少有4小时的间隔。实验组包括对照组（Con），妊娠暴露（AS），孕前暴露（SA），和孕前+妊娠暴露（SS）。肺功能测试（Penh，PAU,TVb,EF50，Tr）在7周时对雄性后代进行。组织病理学,电子显微镜，和蛋白质水平的变化进行了检查。
结果：肺功能测试显示，PAU,TVb,在所有暴露场景中后代的EF50和Tr。具体来说,AS在后代中经历了显著的肺功能损害和线粒体功能障碍,明显的肺部病变和细胞凋亡增加。SA显示相似或甚至更严重的肺功能损害和细胞凋亡。SS表现出最明显的效果，肺功能障碍程度最高，线粒体损伤，和凋亡。组织病理学分析显示暴露于母体CSE的后代有肺部病变。流式细胞术显示子代肺细胞凋亡增加，线粒体膜电位降低。电子显微镜证实线粒体功能障碍。在暴露于母体CSE的后代肺组织中发现了凋亡蛋白的上调和抗凋亡蛋白Bcl-2的下调。
结论：母亲吸烟会导致肺功能受损，肺部病变,和后代的线粒体功能障碍，无论曝光时间和持续时间。此外,它改变了子代肺组织中凋亡相关蛋白的表达，可能导致COPD易感性。
方法：使用雌性C57BL/6J小鼠，建立母体香烟烟雾暴露(CSE)模型。小鼠暴露于香烟烟雾2小时/天，7天/周,曝光之间至少有4小时的间隔。实验组包括对照组（Con），妊娠暴露（AS），孕前暴露（SA），和孕前+妊娠暴露（SS）。肺功能测试（Penh，PAU,TVb,EF50，Tr）在7周时对雄性后代进行。组织病理学,电子显微镜，和蛋白质水平的变化进行了检查。
结果：肺功能测试显示，PAU,TVb,在所有暴露场景中后代的EF50和Tr。具体来说,AS在后代中经历了显著的肺功能损害和线粒体功能障碍,明显的肺部病变和细胞凋亡增加。SA显示相似或甚至更严重的肺功能损害和细胞凋亡。SS表现出最明显的效果，肺功能障碍程度最高，线粒体损伤，和凋亡。组织病理学分析显示暴露于母体CSE的后代有肺部病变。流式细胞术显示子代肺细胞凋亡增加，线粒体膜电位降低。电子显微镜证实线粒体功能障碍。在暴露于母体CSE的后代肺组织中发现了凋亡蛋白的上调和抗凋亡蛋白Bcl-2的下调。
结论：母亲吸烟会导致肺功能受损，肺部病变,和后代的线粒体功能障碍，无论曝光时间和持续时间。此外,它改变了子代肺组织中凋亡相关蛋白的表达，可能导致COPD易感性。
