Particulate matter (PM) of 10‐μm‐sized fine dust in the air penetrates the respiratory tract and contributes to the increasing incidence of various lung diseases, but its definite mechanism is not known. Recently, polydeoxyribonucleotide (PDRN) has been shown to have anti‐inflammatory and regenerative effects in various tissues. However, the bronchial‐related mechanism is not well‐understood. Hence, this experiment is intended to demonstrate the beneficial effect of PDRN administration on PM10‐induced injury in human bronchial‐derived NCI‐H358 cells. To confirm the protective effect of PDRN, PM10 was applied after PDRN pretreatment to confirm changes in NCI‐H358 cells. Experiments were conducted to measure cell survival, cytotoxicity, inflammation, and apoptotic factor changes. WST‐8 assay was used to confirm cell viability, and lactate dehydrogenase assay was used to obtain cytotoxicity. In addition, changes in inflammatory cytokines and apoptotic factors were confirmed by enzyme‐linked immunosorbent assay and Western blot. Decreased cell viability and increased cytotoxicity, inflammatory cytokines, and apoptotic factors were observed after exposure to PM10. However, pretreatment with PDRN enhanced cell viability and reduced cytotoxicity. In addition, the expression of inflammatory cytokines such as tumor necrosis factor‐α, interleukin‐6 (IL‐6), and IL‐1β, and cell death factors such as Apaf‐1, cyt c, caspase‐3, caspase‐9, Bid, and Bax/Bcl‐2 ratio were decreased by PDRN administration in PM10‐exposed NCI‐H358 cells. PDRN, an A2AR agonist, affects cAMP activation and regulation of phosphorylation of PKA and CREB. In addition, treatment with A2AR antagonist 3,7‐dimethyl‐1‐propargylxanthine significantly blocked PDRN's effect. These anti‐cytotoxicity, anti‐inflammation, and anti‐apoptosis effects of PDRN can be attributed to the adenosine A2AR enhancing effect on PM10‐exposed bronchial cells.

中文翻译：

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多脱氧核糖核苷酸对人支气管细胞中颗粒物（PM10）损伤诱导的炎性细胞因子和凋亡因子的减弱作用

空气中10微米大小的细粉尘颗粒物（PM）穿透呼吸道，导致各种肺部疾病的发病率增加，但其确切机理尚不清楚。最近，聚脱氧核糖核苷酸（PDRN）已被证明在各种组织中具有抗炎和再生作用。但是，与支气管相关的机制尚未得到很好的理解。因此，本实验旨在证明PDRN给药对PM10诱导的人支气管NCI-H358细胞损伤的有益作用。为了证实PDRN的保护作用，在PDRN预处理后应用PM10以确认NCI-H358细胞的变化。进行实验以测量细胞存活，细胞毒性，炎症和凋亡因子变化。WST-8分析用于确认细胞活力，乳酸脱氢酶法检测细胞毒性。此外，通过酶联免疫吸附测定和蛋白质印迹证实了炎性细胞因子和凋亡因子的变化。暴露于PM10后，观察到细胞活力降低，细胞毒性，炎性细胞因子和凋亡因子增加。但是，PDRN预处理可增强细胞活力并降低细胞毒性。此外，炎症细胞因子如肿瘤坏死因子α，白介素6（IL-6）和IL-1β的表达以及细胞死亡因子如Apaf-1，cyt c，caspase-3，caspase-9的表达，PMid暴露的NCI-H358细胞中通过PDRN施用可降低Bid，Bid和Bax / Bcl-2比率。PDRN是一种A2AR激动剂，影响cAMP的激活以及PKA和CREB磷酸化的调节。此外，用A2AR拮抗剂3治疗，7-二甲基-1-炔丙基黄嘌呤可显着阻断PDRN的作​​用。PDRN的这些抗细胞毒性，抗发炎和抗凋亡作用可以归因于腺苷A2AR对暴露于PM10的支气管细胞的增强作用。