{"title":"β-榄香烯可减轻香烟烟雾引发的人类支气管上皮细胞炎症、凋亡和氧化应激，并抑制 PI3K/AKT/mTOR 信号通路。","authors":"Yan Li, Li Zhang","doi":"10.15586/aei.v52i6.1199","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a grievous disease that adversely affects human health and life. β-elemene is a type of sesquiterpenoid extracted from <i>Curcuma wenyujin</i> (Zingiberaceae) and displays effects on suppressing tumor growth. However, the regulatory impact of β-elemene in COPD development is not reported.</p><p><strong>Objective: </strong>This study explored the functioning of β-elemene in the progression of COPD.</p><p><strong>Material and methods: </strong>The cell survival rate was confirmed through Cell Counting Kit-8 (CCK-8) assay. The cell apoptosis was evaluated through flow cytometry. The protein expressions were examined through western blot. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS) were examined through the corresponding commercial kits. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were inspected through Enzyme-Linked Immunosorbent Assay (ELISA).</p><p><strong>Results: </strong>The study demonstrated that β-elemene exaggerated cell viability and reduced cell apoptosis in BEAS-2B human bronchial epithelial cell line stimulated by cigarette smoke extract (CSE). Oxidative stress was heightened after 5% CSE induction, but this impact was counteracted by β-elemene treatment. In addition, enhancive inflammation induced by cigarette smoke was attenuated by β-elemene treatment. Finally, our results indicated that the triggered the phosphatidylinositol 3-kinase-protein kinase B-mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway mediated by cigarette smoke was refrained by β-elemene treatment.</p><p><strong>Conclusion: </strong>It was concluded that β-elemene reduced cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cell line, and refrained PI3K/AKT/mTOR signaling pathway. This study proposed that β-elemene could act as a hopeful drug for the treatment of COPD.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":"52 6","pages":"79-84"},"PeriodicalIF":2.5000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Beta-elemene alleviates cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cells, and refrains the PI3K/AKT/mTOR signaling pathway.\",\"authors\":\"Yan Li, Li Zhang\",\"doi\":\"10.15586/aei.v52i6.1199\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a grievous disease that adversely affects human health and life. β-elemene is a type of sesquiterpenoid extracted from <i>Curcuma wenyujin</i> (Zingiberaceae) and displays effects on suppressing tumor growth. However, the regulatory impact of β-elemene in COPD development is not reported.</p><p><strong>Objective: </strong>This study explored the functioning of β-elemene in the progression of COPD.</p><p><strong>Material and methods: </strong>The cell survival rate was confirmed through Cell Counting Kit-8 (CCK-8) assay. The cell apoptosis was evaluated through flow cytometry. The protein expressions were examined through western blot. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS) were examined through the corresponding commercial kits. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were inspected through Enzyme-Linked Immunosorbent Assay (ELISA).</p><p><strong>Results: </strong>The study demonstrated that β-elemene exaggerated cell viability and reduced cell apoptosis in BEAS-2B human bronchial epithelial cell line stimulated by cigarette smoke extract (CSE). Oxidative stress was heightened after 5% CSE induction, but this impact was counteracted by β-elemene treatment. In addition, enhancive inflammation induced by cigarette smoke was attenuated by β-elemene treatment. Finally, our results indicated that the triggered the phosphatidylinositol 3-kinase-protein kinase B-mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway mediated by cigarette smoke was refrained by β-elemene treatment.</p><p><strong>Conclusion: </strong>It was concluded that β-elemene reduced cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cell line, and refrained PI3K/AKT/mTOR signaling pathway. This study proposed that β-elemene could act as a hopeful drug for the treatment of COPD.</p>\",\"PeriodicalId\":7536,\"journal\":{\"name\":\"Allergologia et immunopathologia\",\"volume\":\"52 6\",\"pages\":\"79-84\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2024-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Allergologia et immunopathologia\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.15586/aei.v52i6.1199\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Allergologia et immunopathologia","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.15586/aei.v52i6.1199","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ALLERGY","Score":null,"Total":0}
引用次数: 0
摘要
背景：慢性阻塞性肺疾病（COPD）是一种严重影响人类健康和生命的疾病。β-榄香烯是从姜黄科植物莪术中提取的一种倍半萜类化合物，具有抑制肿瘤生长的作用。然而，β-榄香烯对慢性阻塞性肺病发展的调节作用尚未见报道：本研究探讨了β-榄香烯在慢性阻塞性肺病发展过程中的作用：通过细胞计数试剂盒-8（CCK-8）检测法确认细胞存活率。通过流式细胞术评估细胞凋亡。蛋白质表达通过 Western 印迹进行检测。通过相应的商业试剂盒检测丙二醛（MDA）、超氧化物歧化酶（SOD）和活性氧（ROS）的水平。通过酶联免疫吸附试验（ELISA）检测肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和 IL-1β 的水平：研究结果表明，β-榄香烯能提高受香烟烟雾提取物（CSE）刺激的 BEAS-2B 人支气管上皮细胞系的细胞活力，减少细胞凋亡。5%的CSE诱导后氧化应激增加，但β-榄香烯处理可抵消这种影响。此外，香烟烟雾诱导的增强性炎症也因β-榄香烯处理而减弱。最后，我们的研究结果表明，β-榄香烯能抑制香烟烟雾介导的磷脂酰肌醇3-激酶-蛋白激酶B-雷帕霉素机械靶标（PI3K/AKT/mTOR）通路：结论：β-榄香烯能减少香烟烟雾引发的炎症、细胞凋亡和氧化应激，并抑制 PI3K/AKT/mTOR 信号通路。这项研究认为，β-榄香烯有望成为治疗慢性阻塞性肺病的药物。
Beta-elemene alleviates cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cells, and refrains the PI3K/AKT/mTOR signaling pathway.
Background: Chronic obstructive pulmonary disease (COPD) is a grievous disease that adversely affects human health and life. β-elemene is a type of sesquiterpenoid extracted from Curcuma wenyujin (Zingiberaceae) and displays effects on suppressing tumor growth. However, the regulatory impact of β-elemene in COPD development is not reported.
Objective: This study explored the functioning of β-elemene in the progression of COPD.
Material and methods: The cell survival rate was confirmed through Cell Counting Kit-8 (CCK-8) assay. The cell apoptosis was evaluated through flow cytometry. The protein expressions were examined through western blot. The levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS) were examined through the corresponding commercial kits. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were inspected through Enzyme-Linked Immunosorbent Assay (ELISA).
Results: The study demonstrated that β-elemene exaggerated cell viability and reduced cell apoptosis in BEAS-2B human bronchial epithelial cell line stimulated by cigarette smoke extract (CSE). Oxidative stress was heightened after 5% CSE induction, but this impact was counteracted by β-elemene treatment. In addition, enhancive inflammation induced by cigarette smoke was attenuated by β-elemene treatment. Finally, our results indicated that the triggered the phosphatidylinositol 3-kinase-protein kinase B-mechanistic target of rapamycin (PI3K/AKT/mTOR) pathway mediated by cigarette smoke was refrained by β-elemene treatment.
Conclusion: It was concluded that β-elemene reduced cigarette smoke-triggered inflammation, apoptosis, and oxidative stress in human bronchial epithelial cell line, and refrained PI3K/AKT/mTOR signaling pathway. This study proposed that β-elemene could act as a hopeful drug for the treatment of COPD.
期刊介绍：
Founded in 1972 by Professor A. Oehling, Allergologia et Immunopathologia is a forum for those working in the field of pediatric asthma, allergy and immunology. Manuscripts related to clinical, epidemiological and experimental allergy and immunopathology related to childhood will be considered for publication. Allergologia et Immunopathologia is the official journal of the Spanish Society of Pediatric Allergy and Clinical Immunology (SEICAP) and also of the Latin American Society of Immunodeficiencies (LASID). It has and independent international Editorial Committee which submits received papers for peer-reviewing by international experts. The journal accepts original and review articles from all over the world, together with consensus statements from the aforementioned societies. Occasionally, the opinion of an expert on a burning topic is published in the "Point of View" section. Letters to the Editor on previously published papers are welcomed. Allergologia et Immunopathologia publishes 6 issues per year and is included in the major databases such as Pubmed, Scopus, Web of Knowledge, etc.
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