Pratomo Irandi Putra, Tedjo Aryo, Noor Dimas R
Department of Pulmonology and Respiratory Medicine, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia.
Pulmonology and Respiratory Medicine Staff Group, Universitas Indonesia Hospital, Universitas Indonesia, Depok, Indonesia.
Int J Inflam. 2023 Mar 3;2023:4251299. doi: 10.1155/2023/4251299. eCollection 2023.
Cigarette smoke (CS) was known for its effect of increasing oxidative stress that could trigger tissue injury and endothelial dysfunction mediated by free radicals and reactive oxygen species (ROS). ROS itself is a key signaling molecule that plays a role in the development of inflammatory disorders. Nuclear factor erythroid2 related factor2 (Nrf2) is the main regulator of antioxidant cellular response to cell and tissue-destroying components caused by CS. Nrf2 protein that is significantly activated in the smokers' small airway epithelium is followed by a series of gene expression changes in the same cells. This study aims to observe differentially expressed genes (DEGs) in the human small airway epithelium of smokers compared to genes whose expression changes due to astaxanthin (AST) treatment, an antioxidant compound that can modulate Nrf2. Gene expression data that was stored in the GEO browser (GSE 11952) was analyzed using GEO2R to search for DEG among smokers and nonsmokers subject. DEG was further compared to those genes whose expression changes due to astaxanthin treatment (AST) that were obtained from the Comparative Toxicogenomics Database (CTD; https://ctdbase.org/). DEG ( < 0.05) analysis result shows that there are 23 genes whose expression regulation is reversed compared to gene expression due to AST treatment. The gene function annotations of the 23 DEGs showed the involvement of some of these genes in chemical and oxidative stress, reactive oxygen species (ROS), and apoptotic signaling pathways. All of the genes were involved/associated with chronic bronchitis, adenocarcinoma of the lung, non-small-cell lung carcinoma, carcinoma, small cell lung carcinoma, type 2 diabetes mellitus, emphysema, ischemic stroke, lung diseases, and inflammation. Thus, AST treatment for smokers could potentially decrease the development of ROS and oxidative stress that leads to inflammation and health risks associated with smoking.
香烟烟雾（CS）因其增加氧化应激的作用而闻名，氧化应激可引发由自由基和活性氧（ROS）介导的组织损伤和内皮功能障碍。ROS本身是一种关键的信号分子，在炎症性疾病的发展中起作用。核因子红细胞2相关因子2（Nrf2）是细胞对抗由CS引起的细胞和组织破坏成分的抗氧化反应的主要调节因子。在吸烟者的小气道上皮中显著激活的Nrf2蛋白，随后在同一细胞中发生一系列基因表达变化。本研究旨在观察吸烟者人小气道上皮中差异表达基因（DEGs），并与因虾青素（AST）处理而表达发生变化的基因进行比较，虾青素是一种可调节Nrf2的抗氧化化合物。使用GEO2R分析存储在GEO浏览器（GSE 11952）中的基因表达数据，以在吸烟者和非吸烟者受试者中寻找DEG。将DEG进一步与从比较毒理基因组学数据库（CTD；https://ctdbase.org/）获得的因虾青素处理（AST）而表达发生变化的那些基因进行比较。DEG（<0.05）分析结果表明，与因AST处理导致的基因表达相比，有23个基因的表达调控发生了逆转。这23个DEG的基因功能注释显示其中一些基因参与化学和氧化应激、活性氧（ROS）和凋亡信号通路。所有这些基因都与慢性支气管炎、肺癌腺癌、非小细胞肺癌、癌、小细胞肺癌、2型糖尿病、肺气肿、缺血性中风、肺部疾病和炎症有关。因此，对吸烟者进行AST治疗可能会潜在地减少导致炎症和与吸烟相关的健康风险的ROS和氧化应激的发展。
