Asthma is characterized by airway inflammation and remodeling. 2-Undecanone (methyl nonyl ketone), a volatile organic compound originating from Houttuynia cordata, has the potential to ameliorate inflammatory diseases. This study aimed to explore potential benefits of 2-undecanone in asthma. 2-Undecanone (100, 200, or 400 mg/kg) was administered intragastrically to ovalbumin (OVA)-challenged BALB/c mice. Lung tissues were collected to observe histopathological changes, and bronchoalveolar lavage fluid (BALF) was collected for the detection of inflammatory cells and cytokine production. The results showed that 2-undecanone ameliorated OVA-induced pathologic changes of lungs, including reducing inflammatory cell infiltration, goblet cell hyperplasia, and airway smooth muscle thickness. The number of inflammatory cells and the levels of IL-4, IL-5, IL-13, and IgE in BALF were decreased by 2-undecanone in asthmatic mice. Furthermore, abnormal activation of NF-κB pathway in lung tissues of asthmatic mice was impeded by 2-undecanone. In vitro, 2-undecanone (12.5, 25, or 50 µM) suppressed platelet-derived growth factor-BB-induced proliferation and migration of primary airway smooth muscle cells (ASMCs), and inhibited the switching of ASMCs from contractile phenotype to synthetic phenotype. Consistently, 2-undecanone blocked NF-κB activation in ASMCs. Collectively, 2-undecanone relieves asthma through alleviating airway inflammation and remodeling, and this beneficial effect is achieved by inhibiting NF-κB pathway.

中文翻译：

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2-Undecanone 通过抑制 NF-κB 通路减轻哮喘。

哮喘的特征在于气道炎症和重塑。2-Undecanone（甲基壬基酮）是一种源自鱼腥草的挥发性有机化合物，具有改善炎症性疾病的潜力。本研究旨在探讨 2-十一酮对哮喘的潜在益处。将 2-十一酮（100、200 或 400 mg/kg）灌胃给药至卵清蛋白 (OVA) 攻击的 BALB/c 小鼠。收集肺组织观察组织病理学变化，收集支气管肺泡灌洗液（BALF）检测炎症细胞和细胞因子的产生。结果表明，2-十一烷酮可改善 OVA 引起的肺部病理变化，包括减少炎症细胞浸润、杯状细胞增生和气道平滑肌厚度。炎症细胞的数量和 IL-4、IL-5 的水平，哮喘小鼠中的 2-十一酮可降低 BALF 中的 IL-13 和 IgE。此外，2-十一酮阻碍了哮喘小鼠肺组织中 NF-κB 通路的异常激活。在体外，2-十一酮（12.5、25 或 50 µM）抑制血小板衍生生长因子-BB 诱导的初级气道平滑肌细胞 (ASMC) 增殖和迁移，并抑制 ASMC 从收缩表型向合成表型的转变. 一致地，2-十一酮阻断了 ASMC 中的 NF-κB 激活。总的来说，2-十一酮通过减轻气道炎症和重塑来缓解哮喘，而这种有益效果是通过抑制 NF-κB 通路实现的。在体外，2-十一酮（12.5、25 或 50 µM）抑制血小板衍生生长因子-BB 诱导的初级气道平滑肌细胞 (ASMC) 增殖和迁移，并抑制 ASMC 从收缩表型向合成表型的转变. 一致地，2-十一酮阻断了 ASMC 中的 NF-κB 激活。总的来说，2-十一酮通过减轻气道炎症和重塑来缓解哮喘，而这种有益效果是通过抑制 NF-κB 通路实现的。在体外，2-十一酮（12.5、25 或 50 µM）抑制血小板衍生生长因子-BB 诱导的初级气道平滑肌细胞 (ASMC) 增殖和迁移，并抑制 ASMC 从收缩表型向合成表型的转变. 一致地，2-十一酮阻断了 ASMC 中的 NF-κB 激活。总的来说，2-十一酮通过减轻气道炎症和重塑来缓解哮喘，而这种有益效果是通过抑制 NF-κB 通路实现的。