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<p><i>Peucedanum japonicum</i> Thunberg ethanol extract (PJE), a traditional East Asian medicinal herb recognized for its antioxidant and anti-inflammatory activities, was evaluated for its neuroprotective effects against Alzheimer’s disease related pathology. In an amyloid-β₁–₄₂-induced mouse model, oral administration of PJE significantly enhanced cognitive performance, reduced neuroinflammation by decreasing pro-inflammatory cytokines, and inhibited activation of nuclear factor-kappa-B (NF-κB) and mitogen activated protein kinases (MAPKs) signaling pathways. Furthermore, PJE suppressed neuronal apoptosis by regulating the B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein (Bax) ratio and cleaved caspase-3 expression, while promoting neurotrophic support through upregulation of phospho-cAMP response element-binding protein (p-CREB) and brain-derived neurotrophic factor (BDNF). In vitro, PJE attenuated lipopolysaccharide-induced nitric oxide release in BV-2 microglial cells via downregulation of NF-κB and MAPKs pathways. In SH-SY5Y neuroblastoma cells exposed to H₂O₂, PJE restored cell viability by elevating glutathione content and BDNF expression, increasing the Bcl-2/Bax ratio, and lowering levels of cleaved caspase-9. Overall, these findings demonstrate that PJE confers neuroprotection through a combination of anti-inflammatory, antioxidant, and anti-apoptotic mechanisms, indicating its promise as a natural therapeutic agent for memory and cognitive dysfunction.</p>

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Neuroprotective effects of Peucedanum japonicum Thunberg extract in memory-impaired mice: anti-inflammatory, anti-apoptotic, and in vitro antioxidant actions

  • 期刊论文

  • 发表日期：

    2026年2月26日

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  • Da-Eun Min,
  • Sung-Kwon Lee,
  • Eunji Kim,
  • Bong-Keun Choi,
  • Young-Seob Lee,
  • Hyeong Jun Kim,
  • Seung Hwan Yang

摘要

Peucedanum japonicum Thunberg ethanol extract (PJE), a traditional East Asian medicinal herb recognized for its antioxidant and anti-inflammatory activities, was evaluated for its neuroprotective effects against Alzheimer’s disease related pathology. In an amyloid-β₁–₄₂-induced mouse model, oral administration of PJE significantly enhanced cognitive performance, reduced neuroinflammation by decreasing pro-inflammatory cytokines, and inhibited activation of nuclear factor-kappa-B (NF-κB) and mitogen activated protein kinases (MAPKs) signaling pathways. Furthermore, PJE suppressed neuronal apoptosis by regulating the B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein (Bax) ratio and cleaved caspase-3 expression, while promoting neurotrophic support through upregulation of phospho-cAMP response element-binding protein (p-CREB) and brain-derived neurotrophic factor (BDNF). In vitro, PJE attenuated lipopolysaccharide-induced nitric oxide release in BV-2 microglial cells via downregulation of NF-κB and MAPKs pathways. In SH-SY5Y neuroblastoma cells exposed to H₂O₂, PJE restored cell viability by elevating glutathione content and BDNF expression, increasing the Bcl-2/Bax ratio, and lowering levels of cleaved caspase-9. Overall, these findings demonstrate that PJE confers neuroprotection through a combination of anti-inflammatory, antioxidant, and anti-apoptotic mechanisms, indicating its promise as a natural therapeutic agent for memory and cognitive dysfunction.