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<p>Traumatic brain injury (TBI) induces complex secondary damage, including blood-brain barrier (BBB) disruption, neuroinflammation, and synaptic dysfunction. However, TBI currently lacks effective treatments. This study investigated the neuroprotective effects and mechanisms of Ganoderic acid A (GAA), a triterpenoid from <i>Ganoderma lucidum</i>, in TBI mice and H₂O₂-induced BV-2 microglial cells. Results demonstrated that GAA treatment significantly preserved BBB integrity by reducing Evans blue extravasation, brain edema, and MMP-9 expression, while up-regulating tight junction proteins (ZO-1, Occludin, Claudin-5). GAA attenuated neuroinflammation by inhibiting microglial/astrocytic activation, promoting a shift from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype, and modulating cytokine levels. Furthermore, GAA enhanced synaptic plasticity, increased dendritic spine density, up-regulated PSD95 and SYN expression, and reduced neuronal loss. In vitro, GAA mitigated oxidative stress and inflammation in BV-2 cells. Consequently, GAA improved functional recovery, alleviating anxiety-like behavior and spatial memory deficits in TBI mice. These findings demonstrate that GAA is a multi-target therapeutic candidate for TBI, acting via mechanisms of BBB protection, anti-inflammation, antioxidant activity, and synaptic restoration.</p> Graphical Abstract <p></p>

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Ganoderic Acid a Promotes Functional Recovery After Traumatic Brain Injury By Protecting Blood-brain Barrier Integrity and Modulating Microglial Polarization

  • 期刊论文

  • 发表日期：

    2026年4月13日

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  • Jianfei Wu,
  • Yuandong Tang,
  • Yilin Wang,
  • Bo Liu,
  • Maoya Xu,
  • Youguo Tan,
  • Duanfang Cai,
  • Yuanhuai Chen,
  • Jiayue Zeng,
  • Kezhi Liu,
  • Yu Liu

摘要

Traumatic brain injury (TBI) induces complex secondary damage, including blood-brain barrier (BBB) disruption, neuroinflammation, and synaptic dysfunction. However, TBI currently lacks effective treatments. This study investigated the neuroprotective effects and mechanisms of Ganoderic acid A (GAA), a triterpenoid from Ganoderma lucidum, in TBI mice and H₂O₂-induced BV-2 microglial cells. Results demonstrated that GAA treatment significantly preserved BBB integrity by reducing Evans blue extravasation, brain edema, and MMP-9 expression, while up-regulating tight junction proteins (ZO-1, Occludin, Claudin-5). GAA attenuated neuroinflammation by inhibiting microglial/astrocytic activation, promoting a shift from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype, and modulating cytokine levels. Furthermore, GAA enhanced synaptic plasticity, increased dendritic spine density, up-regulated PSD95 and SYN expression, and reduced neuronal loss. In vitro, GAA mitigated oxidative stress and inflammation in BV-2 cells. Consequently, GAA improved functional recovery, alleviating anxiety-like behavior and spatial memory deficits in TBI mice. These findings demonstrate that GAA is a multi-target therapeutic candidate for TBI, acting via mechanisms of BBB protection, anti-inflammation, antioxidant activity, and synaptic restoration.

Graphical Abstract