Particulate matter (PM) is a type of air pollutant that induces adverse health effects, including acute exacerbation of chronic obstructive pulmonary disease (COPD). However, the effects of co-exposure to PM and cigarette smoke extract (CSE) on bronchial epithelial cells remain unknown. This study investigated the cytotoxic and pro-inflammatory effects of combined exposure to PM and CSE on bronchial epithelial cells, and assessed the potential of antioxidants to inhibit CSE/PM-induced oxidative stress and inflammation. Exposure of epithelial cells to PM or CSE induced cytotoxicity, inflammation, and oxidative stress, all of which were dramatically increased when cells were exposed to the combination of CSE and PM. Importantly, the adverse effects of CSE/PM exposure were suppressed when cells were treated with sulforaphane (SFN) or sulforaphane N-acetylcysteine (SFNAC). Furthermore, SFN and SFNAC suppressed the CSE/PM-induced pro-inflammatory cytokine production and expression of inflammatory genes. Combined PM and CSE exposure further activated the MAPK and Nrf2 signaling pathways. SFN and SFNAC attenuated CSE/PM-induced epithelial toxicity through the ERK/JNK signaling pathway-dependent inhibition of inflammation. Moreover, SFN and SFNAC suppressed ROS generation by activating antioxidant enzymes and Nrf2 signaling. Therefore, SFN and SFNAC could be a promising approach to prevent or mitigate the exacerbation of pulmonary diseases caused by PM and other air pollutants.

中文翻译：

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抗氧化剂对暴露于颗粒物和香烟烟雾提取物的人支气管上皮细胞氧化应激和炎症反应的影响。

颗粒物（PM）是一种空气污染物，会引起不利的健康影响，包括慢性阻塞性肺疾病（COPD）的急性加重。然而，同时暴露于PM和香烟烟雾提取物（CSE）对支气管上皮细胞的影响仍然未知。这项研究调查了PM和CSE联合暴露对支气管上皮细胞的细胞毒性和促炎作用，并评估了抗氧化剂抑制CSE / PM诱导的氧化应激和炎症的潜力。上皮细胞暴露于PM或CSE会诱导细胞毒性，炎症和氧化应激，当细胞暴露于CSE和PM的组合时，所有这些都会急剧增加。重要的，当用萝卜硫烷（SFN）或萝卜硫烷N-乙酰半胱氨酸（SFNAC）处理细胞时，CSE / PM暴露的不良反应得到抑制。此外，SFN和SFNAC抑制了CSE / PM诱导的促炎细胞因子的产生和炎症基因的表达。PM和CSE的联合暴露进一步激活了MAPK和Nrf2信号通路。SFN和SFNAC通过ERK / JNK信号通路依赖性的炎症抑制作用减弱了CSE / PM诱导的上皮毒性。此外，SFN和SFNAC通过激活抗氧化剂酶和Nrf2信号转导抑制了ROS的产生。因此，SFN和SFNAC可能是预防或减轻由PM和其他空气污染物引起的肺部疾病恶化的有前途的方法。SFN和SFNAC抑制了CSE / PM诱导的促炎性细胞因子的产生和炎症基因的表达。PM和CSE的联合暴露进一步激活了MAPK和Nrf2信号通路。SFN和SFNAC通过ERK / JNK信号通路依赖性的炎症抑制作用减弱了CSE / PM诱导的上皮毒性。此外，SFN和SFNAC通过激活抗氧化剂酶和Nrf2信号转导抑制了ROS的产生。因此，SFN和SFNAC可能是预防或减轻由PM和其他空气污染物引起的肺部疾病恶化的有前途的方法。SFN和SFNAC抑制了CSE / PM诱导的促炎性细胞因子的产生和炎症基因的表达。PM和CSE的联合暴露进一步激活了MAPK和Nrf2信号通路。SFN和SFNAC通过ERK / JNK信号通路依赖性的炎症抑制作用减弱了CSE / PM诱导的上皮毒性。此外，SFN和SFNAC通过激活抗氧化剂酶和Nrf2信号转导抑制了ROS的产生。因此，SFN和SFNAC可能是预防或减轻由PM和其他空气污染物引起的肺部疾病恶化的有前途的方法。SFN和SFNAC通过ERK / JNK信号通路依赖性的炎症抑制作用减弱了CSE / PM诱导的上皮毒性。此外，SFN和SFNAC通过激活抗氧化剂酶和Nrf2信号转导抑制了ROS的产生。因此，SFN和SFNAC可能是预防或减轻由PM和其他空气污染物引起的肺部疾病加重的有前途的方法。SFN和SFNAC通过ERK / JNK信号通路依赖性的炎症抑制作用减弱了CSE / PM诱导的上皮毒性。此外，SFN和SFNAC通过激活抗氧化剂酶和Nrf2信号转导抑制了ROS的产生。因此，SFN和SFNAC可能是预防或减轻由PM和其他空气污染物引起的肺部疾病恶化的有前途的方法。