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Objective <p>Gardeniae Fructus (GF), the dried fruit of <i>Gardenia jasminoides</i> J. Ellis, has been used in East Asian medicine for centuries. Its carbonized form, Gardeniae Fructus Carbonisatus (GFC), is produced through processing, yet the effects of this transformation on active constituents and neuroprotective mechanisms remain unclear. This study aims to elucidate the key compositional changes induced by processing and explore their relevance to neuroprotective activity.</p> Methods <p>After obtaining GF and GFC extracts via CO₂ supercritical fluid extraction (SFE), UPLC-Q-TOF-MS/MS was employed for qualitative analysis of differential compounds. A pathology-specific network pharmacology screening approach, combined with UPLC-UV-DAD, was applied to quantify major bioactive differential components. Finally,<i> in vitro</i> models and molecular pharmacology techniques were utilized to validate the neuroprotective effects of key compounds.</p> Results <p>We identified 23 differential compounds and quantified 10 key bioactive constituents. Integrated network pharmacology and quantitative analysis implicated neuroinflammation and ferroptosis in GF’s neuroprotection, with geniposide and crocetin as pivotal compounds. Mechanistic studies confirmed roles for TLR4/NF-κB and Nrf2 pathways.</p> Conclusion <p>Geniposide and Crocetin were identified as key compounds responsible for the neuroprotective effects of GF and GFC, primarily through the inhibition of neuroinflammation and ferroptosis. Crocetin is highlighted as a potential marker for GFC.</p> Graphical Abstract <p> Processing transforms Gardeniae Fructus into GFC, enhancing glycoside–aglycone conversion and markedly increasing crocetin. Integrated network pharmacology and quantitative analysis reveal geniposide and crocetin as core neuroprotective agents.<i> In vitro</i> analysis, these compounds inhibit neuroinflammation and ferroptosis via TLR4/NF-κB suppression and Nrf2 activation, supporting crocetin as a characteristic marker of GFC.</p>

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Processing-induced changes in neuroprotective components and mechanisms of gardeniae fructus: integrating UPLC-Q-TOF-MS/MS, network pharmacology, and in vitro analysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月27日

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  • Le Sun,
  • Ziyu Hou,
  • Wenjie Wang,
  • Peiling Wu,
  • Pei Ma,
  • Jiali Huang,
  • Leyang Fan ,
  • Lijia Xu,
  • Haibo Liu,
  • Peigen Xiao

摘要

Objective

Gardeniae Fructus (GF), the dried fruit of Gardenia jasminoides J. Ellis, has been used in East Asian medicine for centuries. Its carbonized form, Gardeniae Fructus Carbonisatus (GFC), is produced through processing, yet the effects of this transformation on active constituents and neuroprotective mechanisms remain unclear. This study aims to elucidate the key compositional changes induced by processing and explore their relevance to neuroprotective activity.

Methods

After obtaining GF and GFC extracts via CO₂ supercritical fluid extraction (SFE), UPLC-Q-TOF-MS/MS was employed for qualitative analysis of differential compounds. A pathology-specific network pharmacology screening approach, combined with UPLC-UV-DAD, was applied to quantify major bioactive differential components. Finally, in vitro models and molecular pharmacology techniques were utilized to validate the neuroprotective effects of key compounds.

Results

We identified 23 differential compounds and quantified 10 key bioactive constituents. Integrated network pharmacology and quantitative analysis implicated neuroinflammation and ferroptosis in GF’s neuroprotection, with geniposide and crocetin as pivotal compounds. Mechanistic studies confirmed roles for TLR4/NF-κB and Nrf2 pathways.

Conclusion

Geniposide and Crocetin were identified as key compounds responsible for the neuroprotective effects of GF and GFC, primarily through the inhibition of neuroinflammation and ferroptosis. Crocetin is highlighted as a potential marker for GFC.

Graphical Abstract

Processing transforms Gardeniae Fructus into GFC, enhancing glycoside–aglycone conversion and markedly increasing crocetin. Integrated network pharmacology and quantitative analysis reveal geniposide and crocetin as core neuroprotective agents. In vitro analysis, these compounds inhibit neuroinflammation and ferroptosis via TLR4/NF-κB suppression and Nrf2 activation, supporting crocetin as a characteristic marker of GFC.