Chrysene, one of the basic polycyclic aromatic hydrocarbons (PAHs), has been reported to make damages to human health and living environment. Chronic obstructive pulmonary disease (COPD) is a progressive disorder with high morbidity and mortality. To investigate the role of chrysene in the development of COPD, male C57BL/6 mice were exposed to the cigarette smoke (CS) followed with the administration of chrysene. Morphological analyses indicated that chrysene caused earlier and severer pathological changes in CS-exposed mice. Besides, CS-exposed mice with chrysene treatment showed obvious collagen deposition, elevated α-smooth muscle actin (α-SMA) expression and reduced E-cadherin abundance at earlier stage, which suggested the acceleration and aggravation of pulmonary fibrosis. Moreover, quantification of leukocytes and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues implied that chrysene significantly exacerbated the proceeding of inflammation in CS-exposed mice. Furthermore, significantly increased apoptotic rates, augmented expressions of apoptotic related proteins and highly expressed TRPV1 were determined in CS-exposed mice with chrysene treatment, which indicated the association between COPD pathogenesis and TRPV1 channel. In summary, our findings elucidate that chrysene accelerates the development of COPD in a murine model with new molecular mechanisms.

据报道，屈是一种基本的多环芳烃 (PAHs)，会对人类健康和生活环境造成损害。慢性阻塞性肺疾病 (COPD) 是一种具有高发病率和死亡率的进行性疾病。为了研究 chrysene 在 COPD 发展中的作用，将雄性 C57BL/6 小鼠暴露于香烟烟雾 (CS) 中，然后施用 chrysene。形态学分析表明，chrysene 在 CS 暴露的小鼠中引起更早和更严重的病理变化。此外，CS暴露小鼠在早期表现出明显的胶原沉积，α-平滑肌肌动蛋白（α-SMA）表达升高和E-钙粘蛋白丰度降低，这表明肺纤维化加速和加重。而且，支气管肺泡灌洗液 (BALF) 和肺组织中白细胞和促炎细胞因子的量化表明，屈烯显着加剧了 CS 暴露小鼠的炎症进程。此外，在使用 chrysene 处理的 CS 暴露小鼠中确定了显着增加的凋亡率、凋亡相关蛋白的增强表达和高表达的 TRPV1，这表明 COPD 发病机制与 TRPV1 通道之间存在关联。总之，我们的研究结果阐明了 chrysene 在具有新分子机制的小鼠模型中加速了 COPD 的发展。在接受 chrysene 治疗的 CS 暴露小鼠中测定了凋亡相关蛋白的增强表达和高表达的 TRPV1，这表明 COPD 发病机制与 TRPV1 通道之间存在关联。总之，我们的研究结果阐明了 chrysene 在具有新分子机制的小鼠模型中加速了 COPD 的发展。在接受 chrysene 治疗的 CS 暴露小鼠中测定了凋亡相关蛋白的增强表达和高表达的 TRPV1，这表明 COPD 发病机制与 TRPV1 通道之间存在关联。总之，我们的研究结果阐明了 chrysene 在具有新分子机制的小鼠模型中加速了 COPD 的发展。