各种因素均可导致肺损伤和纤维化，这是由于它们的炎症性质，两者都可能导致严重的临床后果。菊花茵陈菊（Inula japonica Thunb.）在传统中药中被用于肺部疾病的治疗。然而，茵陈菊挥发油（EOI）对肺损伤和纤维化的作用和机制尚不清楚。为了调查EOI对博莱霉素（BLM）诱导的急性肺损伤和慢性纤维化形成的治疗效果以及其潜在机制。通过气相色谱-质谱联用法（GC-MS）鉴定EOI中的成分，并使用高效液相色谱（HPLC）制备EOI化合物。使用西方博特和实时定量聚合酶链反应（qPCR）验证EOI及其活性成分对炎症、氧化应激和纤维化信号通路的影响。EOI治疗显著减轻了BLM诱导急性肺损伤小鼠中炎症和氧化应激反应，通过降低肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和丙二醛等炎症和氧化应激因子的水平。EOI治疗还能通过抑制TGF-β/Smad和PI3K/Akt通路，在BLM诱导的肺纤维化小鼠中抑制纤维组织的形成。色谱分析和制备结果表明，EOI中存在脂肪酸和酚类衍生物。根据细胞炎症和纤维化模型，EOI中的酚类化合物可以通过调节NO、TNF-α、IL-6、TGF-β1和α-SMA等促炎和促纤维细胞因子来展示EOI的抗炎和抗纤维化作用。EOI通过抑制炎症反应和调节氧化还原平衡以及介导TGF-β/Smad和PI3K/Akt改善了BLM诱导的小鼠肺损伤和纤维化，表明EOI具有治疗肺部疾病的潜力。版权所有©2023 Elsevier B.V. 发表。

Pulmonary injury and fibrosis can be caused by various factors because of their inflammatory nature, both can lead to serious clinical consequences. Inula japonica Thunb. is used in traditional Chinese medicine for the treatment of lung diseases. However, the effect and mechanism of action of the essential oil of I. japonica (EOI) on pulmonary injury and fibrosis are not well understood.To investigate the therapeutic effects of EOI on mice with bleomycin (BLM)-induced acute pulmonary injury and chronic fibrosis formation, as well as its potential mechanism.A short-term mouse model of pulmonary injury was established by intratracheal injection of BLM to investigate the anti-inflammatory effect of EOI, and a long-term model of pulmonary fibrosis was used to explore the anti-fibrosis effect of EOI. High-dose EOI (200 mg/kg) was administered intragastrically, and low-dose (50 mg/kg) was administered by intratracheal injection. Gas chromatography-mass spectrometry (GC-MS) was used to identify the ingredients in EOI, and high-performance liquid chromatography (HPLC) was performed for the preparation of EOI compounds. Western blot and real-time qPCR were used to verify the effects of EOI and its active composition on inflammation, oxidative stress and fibrosis signaling pathway.Treatment with EOI significantly reduced the inflammation and oxidative stress by reducing the levels of inflammatory and oxidative cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and malondialdehyde in BLM-treated mice with acute pulmonary injury. EOI treatment could also suppress the formation of fibrous tissue in mice with BLM-induced pulmonary fibrosis through inhibiting TGF-β/Smad and PI3K/Akt pathways. Chromatographic analysis and preparation suggested that fatty acid and phenol derivatives are present in EOI. Based on cellular inflammation and fibrosis models, the phenolic compounds in EOI can represent the anti-inflammatory and anti-fibrotic effects of EOI by regulating pro-inflammatory and pro-fibrotic cytokines such as NO, TNF-α, IL-6, TGF-β1, and α-SMA.EOI ameliorated BLM-induced pulmonary injury and fibrosis in mice by inhibiting the inflammatory response and regulating the redox equilibrium, as well as by mediating TGFβ/Smad and PI3K/Akt, which suggested that EOI has potential to treat pulmonary diseases.Copyright © 2023. Published by Elsevier B.V.