Department of Pharmacology, Chiesi Farmaceutici SpA, Parma, Italy.
Ann N Y Acad Sci. 2012 Jul;1259:39-46. doi: 10.1111/j.1749-6632.2012.06531.x.
Acrolein (2-propenal) is a highly reactive α,β-unsaturated aldehyde and a respiratory irritant that is ubiquitously present in the environment but that can also be generated endogenously at sites of inflammation. Acrolein is abundant in tobacco smoke, which is the major environmental risk factor for chronic obstructive pulmonary disease (COPD), and elevated levels of acrolein are found in the lung fluids of COPD patients. Its high electrophilicity makes acrolein notorious for its facile reaction with biological nucleophiles, leading to the modification of proteins and DNA and depletion of antioxidant defenses. As a consequence, acrolein results in oxidative stress as well as altered intracellular signaling and gene transcription/translation. In pulmonary cells, acrolein, at subtoxic concentrations, can activate intracellular stress kinases, alter the production of inflammatory mediators and proteases, modify innate immune response, induce mucus hypersecretion, and damage airway epithelium. A better comprehension of the mechanisms underlying acrolein effects in the airways may suggest novel treatment strategies in COPD.
丙烯醛（2-丙烯醛）是一种具有高反应性的α,β-不饱和醛，也是一种呼吸道刺激性物质，普遍存在于环境中，但也可以在炎症部位内源性产生。丙烯醛在烟草烟雾中含量丰富，而烟草烟雾是慢性阻塞性肺疾病（COPD）的主要环境风险因素，并且在 COPD 患者的肺部液中发现丙烯醛水平升高。其高亲电性使其易于与生物亲核试剂反应，导致蛋白质和 DNA 的修饰以及抗氧化防御的消耗，从而臭名昭著。因此，丙烯醛会导致氧化应激以及细胞内信号转导和基因转录/翻译的改变。在肺细胞中，亚毒性浓度的丙烯醛可以激活细胞内应激激酶，改变炎症介质和蛋白酶的产生，修饰先天免疫反应，诱导黏液过度分泌，并损害气道上皮。更好地理解丙烯醛在气道中的作用机制可能为 COPD 提出新的治疗策略。
