ArticleMolecular neurobiology2026
Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
41504993What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.