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<p>We extracted turmeric volatile oil (TVO) from turmeric using supercritical CO₂ extraction for potential allergic rhinitis (AR) therapy. The volatile components of TVO were analyzed using gas chromatography mass spectrometry and gas chromatography-ion migration spectrometry. The pharmacological effects of TVO on ovalbumin (OVA)-induced AR in mice were evaluated through pathological markers, microbiomics, metabolomics, and proteomics. An inflammatory model using human mast cells (HMCs) was established to assess whether TVO could mitigate inflammation. TVO effectively alleviated AR symptoms in OVA-sensitized mice and reduced inflammation in lipopolysaccharide- and interferon-γ-treated HMCs. TVO suppressed the inflammatory cytokine production, restored the nasal microbiota composition, and regulated serum metabolic profiles. Proteomic analysis using four-dimensional data-independent acquisition indicated that the mitogen-activated protein kinase (MAPK) and transcription factor nuclear factor-κB (NF-κB) signaling pathways are involved in TVO’s anti-inflammatory mechanism. Accordingly, TVO inhibited the activation of MAPK and NF-κB pathways in the OVA mouse model and the inflammatory HMCs model. Jun N-terminal kinase and Relb were identified as key mediators in the therapeutic action of TVO, with <i>Relb</i> knockdown enhancing its anti-inflammatory effect, suggesting that TVO has potential as a therapeutic agent for alleviating AR.</p>

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Multi-omics combined analysis of turmeric volatile oil alleviating allergic rhinitis through the JNK/MAPK-Relb/NF-κB pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月18日

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  • Liying Shang,
  • Shuai Bian,
  • Xin Wang,
  • Yanan Xu,
  • Mingyue Wang,
  • Daqing Zhao,
  • Wei Zhang,
  • Xueyuan Bai

摘要

We extracted turmeric volatile oil (TVO) from turmeric using supercritical CO₂ extraction for potential allergic rhinitis (AR) therapy. The volatile components of TVO were analyzed using gas chromatography mass spectrometry and gas chromatography-ion migration spectrometry. The pharmacological effects of TVO on ovalbumin (OVA)-induced AR in mice were evaluated through pathological markers, microbiomics, metabolomics, and proteomics. An inflammatory model using human mast cells (HMCs) was established to assess whether TVO could mitigate inflammation. TVO effectively alleviated AR symptoms in OVA-sensitized mice and reduced inflammation in lipopolysaccharide- and interferon-γ-treated HMCs. TVO suppressed the inflammatory cytokine production, restored the nasal microbiota composition, and regulated serum metabolic profiles. Proteomic analysis using four-dimensional data-independent acquisition indicated that the mitogen-activated protein kinase (MAPK) and transcription factor nuclear factor-κB (NF-κB) signaling pathways are involved in TVO’s anti-inflammatory mechanism. Accordingly, TVO inhibited the activation of MAPK and NF-κB pathways in the OVA mouse model and the inflammatory HMCs model. Jun N-terminal kinase and Relb were identified as key mediators in the therapeutic action of TVO, with Relb knockdown enhancing its anti-inflammatory effect, suggesting that TVO has potential as a therapeutic agent for alleviating AR.