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<p>Neurodegenerative disorders and age-related cognitive decline remain significant global health challenges, with current therapies offering only symptomatic relief. Flavonoids have emerged as a promising alternative due to their multi-target actions and safety. One such is wogonin (5,7-dihydroxy-8-methoxyflavone), a root-specific flavone from <i>Scutellaria species</i>, which has shown strong neuroprotective potential. This review provides a comprehensive overview of biosynthesis, pharmacokinetics, and mechanistic insights into wogonin, which confer neuroprotection and cognitive resilience. Evidence from cellular and animal models highlights its ability to cross the blood-brain barrier and modulate key signaling pathways, including NF-κB, MAPK, PI3K/Akt, Nrf2/ARE, AMPK, and CREB/BDNF, thereby attenuating oxidative stress, neuroinflammation, mitochondrial dysfunction, and synaptic loss. Furthermore, we summarize preclinical and emerging clinical evidence supporting its role in aging-associated neurodegenerative disorders.</p> Graphical Abstract <p></p>

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Wogonin-mediated modulation of cellular signaling pathways: Mechanistic insights into neuroprotection

  • 期刊论文

  • 发表日期：

    2026年2月18日

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  • Shivani Chib,
  • Kajal Sharma,
  • Bhanu Parsad,
  • Bhaskar Jyoti Dutta,
  • Randhir Singh

摘要

Neurodegenerative disorders and age-related cognitive decline remain significant global health challenges, with current therapies offering only symptomatic relief. Flavonoids have emerged as a promising alternative due to their multi-target actions and safety. One such is wogonin (5,7-dihydroxy-8-methoxyflavone), a root-specific flavone from Scutellaria species, which has shown strong neuroprotective potential. This review provides a comprehensive overview of biosynthesis, pharmacokinetics, and mechanistic insights into wogonin, which confer neuroprotection and cognitive resilience. Evidence from cellular and animal models highlights its ability to cross the blood-brain barrier and modulate key signaling pathways, including NF-κB, MAPK, PI3K/Akt, Nrf2/ARE, AMPK, and CREB/BDNF, thereby attenuating oxidative stress, neuroinflammation, mitochondrial dysfunction, and synaptic loss. Furthermore, we summarize preclinical and emerging clinical evidence supporting its role in aging-associated neurodegenerative disorders.

Graphical Abstract