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<p>Depression is a highly prevalent and disabling mental disorder. Its pathogenesis arises from a complex interplay of interconnected biological systems. This interplay extends well beyond the classical monoamine deficiency framework. This review focuses on four key pathways: monoamine depletion by oxidative degradation and transporter hyperactivity, neuroinflammation from glial crosstalk to STING-GPX4 ferroptosis, gut dysbiosis disrupting barrier integrity and short-chain fatty acids, and impaired neuroplasticity due to brain-derived neurotrophic factor silencing and tropomyosin receptor kinase B disruption. We then map each pathway to bioactive compounds from medicinal-edible plants—flavonoids, alkaloids, saponins, terpenoids, and polysaccharides. These agents exert multi-target, multi-pathway effects: restoring serotonin, dopamine, and norepinephrine; suppressing nuclear factor kappa B/NOD-like receptor protein 3 and microglial activation; activating brain-derived neurotrophic factor/tropomyosin receptor kinase B/mammalian target of rapamycin to repair plasticity; correcting glucocorticoid receptor to balance hypothalamic–pituitary–adrenal axis; and remodeling gut microbiota to produce beneficial metabolites (<i>e.g</i>., short-chain fatty acids, 5-hydroxytryptophan). We also critically assess translational bottlenecks—poor oral bioavailability, single-compound studies lacking formula synergy, insufficient pharmacokinetic-target data, and few rigorous trials. By integrating neurobiology with pharmacognosy, this review provides a framework for developing evidence-based functional foods and adjunctive therapies.</p> Graphical Abstract <p></p>

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Medicinal-Edible Plants in Depression Therapy: Mechanistic Basis, Bioactive Compounds, and Translational Perspectives

  • 期刊论文

  • 发表日期：

    2026年7月18日

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  • Guangyu Zhang,
  • Li Gao,
  • Haixia Ji,
  • Taotao Zhang,
  • Xiaokai Ma,
  • Yinghu Zhao

摘要

Depression is a highly prevalent and disabling mental disorder. Its pathogenesis arises from a complex interplay of interconnected biological systems. This interplay extends well beyond the classical monoamine deficiency framework. This review focuses on four key pathways: monoamine depletion by oxidative degradation and transporter hyperactivity, neuroinflammation from glial crosstalk to STING-GPX4 ferroptosis, gut dysbiosis disrupting barrier integrity and short-chain fatty acids, and impaired neuroplasticity due to brain-derived neurotrophic factor silencing and tropomyosin receptor kinase B disruption. We then map each pathway to bioactive compounds from medicinal-edible plants—flavonoids, alkaloids, saponins, terpenoids, and polysaccharides. These agents exert multi-target, multi-pathway effects: restoring serotonin, dopamine, and norepinephrine; suppressing nuclear factor kappa B/NOD-like receptor protein 3 and microglial activation; activating brain-derived neurotrophic factor/tropomyosin receptor kinase B/mammalian target of rapamycin to repair plasticity; correcting glucocorticoid receptor to balance hypothalamic–pituitary–adrenal axis; and remodeling gut microbiota to produce beneficial metabolites (e.g., short-chain fatty acids, 5-hydroxytryptophan). We also critically assess translational bottlenecks—poor oral bioavailability, single-compound studies lacking formula synergy, insufficient pharmacokinetic-target data, and few rigorous trials. By integrating neurobiology with pharmacognosy, this review provides a framework for developing evidence-based functional foods and adjunctive therapies.

Graphical Abstract