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Archive > Volume 17 Issue 3 > 2025,17(3):539-547. DOI:https://doi.org/10.1016/j.chmed.2024.11.009 Prev Next

神香草提取物通過PI3K/JNK/P38信號通路和脂質(zhì)穩(wěn)態(tài)調(diào)節(jié)抑制OVA致敏的過敏性哮喘

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Hyssopus cuspidatus extract inhibited OVA-sensitized allergic asthma through PI3K/JNK/P38 signaling pathway and lipid homeostasis regulation

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    摘要:
    摘要：目的：研究神香草提取物對卵清蛋白（ovalbumin，OVA）誘導(dǎo)的過敏性哮喘的作用及其分子機(jī)制。方法：使用超高效液相色譜-四極桿-飛行時間質(zhì)譜對神香草提取物的化學(xué)成分進(jìn)行鑒定。通過卵清蛋白致敏小鼠建立哮喘模型，并使用地塞米松作為陽性對照。通過氣道阻力測試、支氣管肺泡灌洗液和外周血中的白細(xì)胞計數(shù)、血清和肺組織中細(xì)胞因子水平測定、以及組織學(xué)檢查來評估神香草提取物對哮喘的治療效果。使用網(wǎng)絡(luò)藥理學(xué)方法預(yù)測作用機(jī)制，應(yīng)用Western blotting和非靶向脂質(zhì)組學(xué)的方法進(jìn)行機(jī)制驗證。結(jié)果：在神香草提取物中共鑒定出52種化合物，主要是萜類和黃酮類。神香草提取物顯著降低了哮喘小鼠的氣道阻力、肺組織中嗜酸性粒細(xì)胞的浸潤以及免疫球蛋白E（IgE）、白細(xì)胞介素-4（IL-4）、白細(xì)胞介素-5（IL-5）和白細(xì)胞介素-13（IL-13）的水平。網(wǎng)絡(luò)藥理學(xué)分析表明，磷脂酰肌醇3激酶（phosphatidylinositol 3-kinases, PI3K）、c-Jun N末端激酶（c-Jun N-terminal kinase, JNK）和p38絲裂原活化蛋白激酶（p38 Mitogen-activated protein kinase, P38）可能是HCE治療過敏性哮喘的關(guān)鍵蛋白。Western blotting結(jié)果顯示，神香草提取物組磷酸化的PI3K、JNK和P38的水平均下調(diào)。此外，神香草提取物顯著上調(diào)了神經(jīng)酰胺（Ceramide, Cer）和鞘磷脂（Sphingomyelin, SM）的水平，并下調(diào)了磷脂酰膽堿（Phosphatidylcholine, PC）的水平。結(jié)論：神香草提取物通過PI3K/JNK/P38信號通路和脂質(zhì)穩(wěn)態(tài)調(diào)節(jié)抑制過敏性哮喘。

    Abstract:
    Objective: To investigate the effect and mechanism of Hyssopus cuspidatus Boriss. extract (HCE) in ovalbumin (OVA)-induced allergic asthma. Methods: Components identification of HCE was conducted using ultra performance liquid chromatography-quadrupole-time of flight-mass spectrometry. Mice were sensitized with OVA to establish asthmatic model, and dexamethasone was used as positive control. Respiratory reactivity, white cells counting in bronchoalveolar lavage fluid and peripheral blood, cytokine level measurement in serum and lung tissue, and histologic examination were performed to evaluate the therapeutic effect of HCE on asthma. Network pharmacology approach was used for mechanism prediction. Western blotting and untargeted lipidomics method were applied for mechanism validation. Results: Fifty-two compounds were identified in HCE, predominantly terpenoids and flavonoids. HCE markedly reduced airway resistance, the eosinophil infiltration in lung tissues, and the levels of immunoglobulin E, interleukin-4, interleukin-5, and interleukin-13. Network pharmacology analysis suggested phosphatidylinositol 3-kinases (PI3K), c-Jun N-terminal kinase (JNK), and p38 Mitogen-activated protein kinase (p38 MAPK) may be key proteins of HCE in the treatment of allergic asthma. Western blot results indicated that the levels of phosphorylated PI3K, JNK, and P38 were downregulated in HCEtreated group. Moreover, HCE significantly upregulated the levels of ceramide and sphingomyelin and downregulated the level of phosphatidylcholine. Conclusion: HCE inhibited allergic asthma via PI3K/JNK/P38 signaling pathway and lipid homeostasis regulation.

    關(guān)鍵詞:
    過敏性哮喘;神香草提取物;脂質(zhì)組學(xué);網(wǎng)絡(luò)藥理學(xué);PI3K/JNK/P38信號通路

    Keywords:


    Project Supported:
    This project was financially supported by National Natural Science Foundation of China (No. 82474186, 31000150) and the Fundamental Research Funds for the Central Universities, HUST (No. 2016YXMS145).

    Clc Number:

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