{"title":"Dihydroartemisinin attenuates PM-induced lung injury by inhibiting inflammation and regulating autophagy.","authors":"Lingjing Liu, Jingli Li, Yincong Xue, Shuying Xie, Nian Dong, Chengshui Chen","doi":"10.3389/fpubh.2025.1548224","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The study investigates the effects and mechanisms of dihydroartemisinin (DHA) in mitigating lung injury induced by particulate matter (PM).</p><p><strong>Methods: </strong>The lung injury model was induced by PM particles <i>in vivo</i> and <i>in vitro</i>. Hematoxylin and Eosin (H&E) staining was utilized for the detection of the thickening of airway wall and the infiltration of inflammatory cells in mouse lung tissue. The expressions of inflammatory factors were detected in alveolar lavage fluid and cell supernatant. TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, Caspase-1, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), microtubule-associated protein 1 light chain 3-II (LC3-II) and Belcin-1 were used to observe the apoptosis and autophagy related expressions in mouse lung tissue, and p-p65 was detected by immunofluorescence.</p><p><strong>Results: </strong>H&E staining revealed DHA alleviates PM-induced lung injury <i>in vivo</i>. Moreover, DHA reduced IL-6, IL-8, and IL-1β levels by ~50% (<i>p</i> < 0.05), highlighting its anti-inflammatory effects. Furthermore, immunohistochemistry showed that DHA treatment inhibited the pro-apoptotic expression of Bax/BCL2 and cleaved-Caspase-3, respectively. In addition, immunofluorescence staining revealed that the LC3-II and Beclin-1 levels dramatically increased in the PM group compared to Control group, but greatly reduced by DHA. Further, we found that DHA inhibited the activation of the NF-KB signaling pathway.</p><p><strong>Conclusion: </strong>DHA protects against PM-induced lung injury through anti-inflammatory, anti-apoptotic, and autophagy-regulating mechanisms, offering a potential drug option for improving PM-induced lung injury.</p>","PeriodicalId":12548,"journal":{"name":"Frontiers in Public Health","volume":"13 ","pages":"1548224"},"PeriodicalIF":3.4000,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925939/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Public Health","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fpubh.2025.1548224","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The study investigates the effects and mechanisms of dihydroartemisinin (DHA) in mitigating lung injury induced by particulate matter (PM).
Methods: The lung injury model was induced by PM particles in vivo and in vitro. Hematoxylin and Eosin (H&E) staining was utilized for the detection of the thickening of airway wall and the infiltration of inflammatory cells in mouse lung tissue. The expressions of inflammatory factors were detected in alveolar lavage fluid and cell supernatant. TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling) staining, Caspase-1, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), microtubule-associated protein 1 light chain 3-II (LC3-II) and Belcin-1 were used to observe the apoptosis and autophagy related expressions in mouse lung tissue, and p-p65 was detected by immunofluorescence.
Results: H&E staining revealed DHA alleviates PM-induced lung injury in vivo. Moreover, DHA reduced IL-6, IL-8, and IL-1β levels by ~50% (p < 0.05), highlighting its anti-inflammatory effects. Furthermore, immunohistochemistry showed that DHA treatment inhibited the pro-apoptotic expression of Bax/BCL2 and cleaved-Caspase-3, respectively. In addition, immunofluorescence staining revealed that the LC3-II and Beclin-1 levels dramatically increased in the PM group compared to Control group, but greatly reduced by DHA. Further, we found that DHA inhibited the activation of the NF-KB signaling pathway.
Conclusion: DHA protects against PM-induced lung injury through anti-inflammatory, anti-apoptotic, and autophagy-regulating mechanisms, offering a potential drug option for improving PM-induced lung injury.
目的：研究双氢青蒿素（DHA）减轻颗粒物（PM）所致肺损伤的作用及其机制。方法：采用PM颗粒在体内和体外诱导肺损伤模型。采用苏木精-伊红（H&E）染色法检测小鼠肺组织气道壁增厚及炎症细胞浸润情况。检测肺泡灌洗液和细胞上清液中炎症因子的表达。TUNEL （Terminal脱氧核苷酸转移酶dUTP nick end labeling）染色、Caspase-1、Bcl-2相关X蛋白（Bax）、b细胞淋巴瘤2 （Bcl-2）、微管相关蛋白1轻链3-II （LC3-II）、Belcin-1观察小鼠肺组织中凋亡和自噬相关表达，免疫荧光检测p-p65。结果：H&E染色显示DHA可减轻pm诱导的肺损伤。此外，DHA可使IL-6、IL-8和IL-1β水平降低约50% (p < 0.05)，显示其抗炎作用。此外，免疫组织化学显示，DHA处理分别抑制Bax/BCL2和cleaved-Caspase-3的促凋亡表达。此外，免疫荧光染色显示PM组LC3-II和Beclin-1水平较对照组显著升高，而DHA则使LC3-II和Beclin-1水平显著降低。此外，我们发现DHA抑制NF-KB信号通路的激活。结论：DHA通过抗炎、抗凋亡和自噬调节机制对pm诱导的肺损伤具有保护作用，为改善pm诱导的肺损伤提供了一种潜在的药物选择。
期刊介绍：
Frontiers in Public Health is a multidisciplinary open-access journal which publishes rigorously peer-reviewed research and is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians, policy makers and the public worldwide. The journal aims at overcoming current fragmentation in research and publication, promoting consistency in pursuing relevant scientific themes, and supporting finding dissemination and translation into practice.
Frontiers in Public Health is organized into Specialty Sections that cover different areas of research in the field. Please refer to the author guidelines for details on article types and the submission process.
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