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<p>Byakangelicol (BYA) is a furanocoumarin extracted from <i>Angelica dahurica</i> and exerts free radical scavenging. However, there are few studies available on the neuroprotective effects of BYA against ischemic brain injury. This research investigated the effects of BYA on ischemic stroke using a photothrombotic ischemia mouse model. Our findings showed that BYA administration observably attenuated brain infarction and neurological deficits during acute cortical injury, confirming by Nissl staining, TUNEL staining, cylinder test, and grid walking test. The neuroprotective effects of BYA were associated with the reduction in microglial activation and inhibition of neuroinflammation, along with the downregulation of TLR3/TLR4/MyD88/SARM1/NF-κB signaling pathways in post-ischemic brains. BYA treatment also decreased the production of 8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE) and elevated the expression of Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), and glutathione peroxidase 1 (GPX1) following ischemic injury. Overall, BYA administration modulates ischemia-induced microglial activation, oxidative stress factors, and antioxidant enzymes in the cortical infarct core, which is closely associated with neuronal protection and improved neurological outcomes after ischemic stroke.</p>

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Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress

  • 期刊论文

  • 发表日期：

    2026年1月8日

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  • Xiao Wan Wang,
  • Yan Qiong Fu,
  • Zhuo Li Li,
  • Ting Li,
  • Hui Lan Wang,
  • Yu Zheng,
  • Chan Zhang,
  • Miaolin Zeng,
  • Chan Li,
  • Dewei Xie,
  • Bai Hui Chen

摘要

Byakangelicol (BYA) is a furanocoumarin extracted from Angelica dahurica and exerts free radical scavenging. However, there are few studies available on the neuroprotective effects of BYA against ischemic brain injury. This research investigated the effects of BYA on ischemic stroke using a photothrombotic ischemia mouse model. Our findings showed that BYA administration observably attenuated brain infarction and neurological deficits during acute cortical injury, confirming by Nissl staining, TUNEL staining, cylinder test, and grid walking test. The neuroprotective effects of BYA were associated with the reduction in microglial activation and inhibition of neuroinflammation, along with the downregulation of TLR3/TLR4/MyD88/SARM1/NF-κB signaling pathways in post-ischemic brains. BYA treatment also decreased the production of 8-hydroxydeoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE) and elevated the expression of Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), and glutathione peroxidase 1 (GPX1) following ischemic injury. Overall, BYA administration modulates ischemia-induced microglial activation, oxidative stress factors, and antioxidant enzymes in the cortical infarct core, which is closely associated with neuronal protection and improved neurological outcomes after ischemic stroke.