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Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress
Xiao Wan Wang1, Yan Qiong Fu1, Zhuo Li Li1
1Department of Histology and Embryology, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Molecular Neurobiology
|January 8, 2026
Summary
Byakangelicol (BYA) protects the brain from ischemic stroke by reducing inflammation and oxidative stress. This furanocoumarin attenuates brain damage and improves neurological function after stroke.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Byakangelicol (BYA), a furanocoumarin from Angelica dahurica, has free radical scavenging properties.
- Limited research exists on BYA's neuroprotective effects against ischemic brain injury.
Purpose of the Study:
- To investigate the neuroprotective potential of BYA in a mouse model of ischemic stroke.
- To elucidate the mechanisms underlying BYA's effects on brain injury, inflammation, and oxidative stress.
Main Methods:
- A photothrombotic ischemia mouse model was used to induce acute cortical injury.
- BYA administration effects were assessed via histological staining (Nissl, TUNEL), behavioral tests (cylinder, grid walking), and molecular pathway analysis.
- Levels of oxidative stress markers (8-OHdG, 4-HNE) and antioxidant enzymes (SOD1, SOD2, GPX1) were measured.
Main Results:
- BYA treatment significantly reduced brain infarction and neurological deficits.
- BYA attenuated microglial activation and neuroinflammation by downregulating TLR3/TLR4/MyD88/SARM1/NF-κB pathways.
- BYA decreased oxidative stress markers and increased antioxidant enzyme expression in post-ischemic brains.
Conclusions:
- BYA demonstrates significant neuroprotective effects against ischemic stroke in mice.
- BYA's mechanism involves modulating microglial activation, neuroinflammation, and oxidative stress.
- BYA administration offers a promising therapeutic strategy for ischemic brain injury.
