Chen Haoming, Li Bing, Cao Hangbing, Zhao Yehong, Zou Yuanjie, Wang Wenyang, Mu Min, Tao Xinrong
Key Laboratory of Industrial Dust Control and Occupational Health of the Ministry of Education, Anhui University of Science and Technology; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, Anhui University of Science and Technology; Anhui Province Engineering Laboratory of Occupational Health and Safety; School of Medicine, Department of Medical Frontier Experimental Center, Anhui University of Science and Technology.
Key Laboratory of Industrial Dust Control and Occupational Health of the Ministry of Education, Anhui University of Science and Technology; Key Laboratory of Industrial Dust Deep Reduction and Occupational Health and Safety of Anhui Higher Education Institutes, Anhui University of Science and Technology; Anhui Province Engineering Laboratory of Occupational Health and Safety; School of Medicine, Department of Medical Frontier Experimental Center, Anhui University of Science and Technology;
J Vis Exp. 2023 Mar 3(193). doi: 10.3791/65127.
Smoking and exposure to silica are common among occupational workers, and silica is more likely to injure the lungs of smokers than non-smokers. The role of nicotine, the primary addictive ingredient in cigarettes, in silicosis development is unclear. The mouse model employed in this study was simple and easily controlled, and it effectively simulated the effects of chronic nicotine ingestion and repeated exposure to silica on lung fibrosis through epithelial-mesenchymal transition in human beings. In addition, this model can help in the direct study of the effects of nicotine on silicosis while avoiding the effects of other components in cigarette smoke. After environmental adaptation, mice were injected subcutaneously with 0.25 mg/kg nicotine solution into the loose skin over the neck every morning and evening at 12 h intervals over 40 days. Additionally, crystalline silica powder (1-5 µm) was suspended in normal saline, diluted to a suspension of 20 mg/mL, and dispersed evenly using an ultrasonic water bath. The isoflurane-anesthetized mice inhaled 50 µL of this silica dust suspension through the nose and were awoken via chest massage. Silica exposure was administrated daily on days 5-19. The double-exposed mouse model was exposed to nicotine and then silica, which matches the exposure history of workers who are exposed to both harmful factors. In addition, nicotine promoted pulmonary fibrosis through epithelial-mesenchymal transformation (EMT) in mice. This animal model can be used to study the effects of multiple factors on the development of silicosis.
吸烟和接触二氧化硅在职业工人中很常见，而且二氧化硅对吸烟者肺部的伤害比对不吸烟者更有可能。香烟中的主要成瘾成分尼古丁在矽肺发展中的作用尚不清楚。本研究中使用的小鼠模型简单且易于控制，它通过人类上皮-间质转化有效地模拟了慢性尼古丁摄入和反复接触二氧化硅对肺纤维化的影响。此外，该模型有助于直接研究尼古丁对矽肺的影响，同时避免香烟烟雾中其他成分的影响。环境适应后，小鼠于40天内每天早晚每隔12小时在颈部松弛皮肤下皮下注射0.25mg/kg尼古丁溶液。此外，将结晶二氧化硅粉末（1-5μm）悬浮于生理盐水中，稀释至20mg/mL的悬浮液，并使用超声水浴均匀分散。用异氟烷麻醉的小鼠通过鼻子吸入50μL这种二氧化硅粉尘悬浮液，并通过胸部按摩唤醒。在第5-19天每天进行二氧化硅暴露。双暴露小鼠模型先接触尼古丁，然后接触二氧化硅，这与同时接触两种有害因素的工人的暴露史相符。此外，尼古丁通过小鼠上皮-间质转化（EMT）促进肺纤维化。这种动物模型可用于研究多种因素对矽肺发展的影响。
