ArticleMolecular neurobiology2023
Network Pharmacology Prediction and Experimental Verification for Anti-Ferroptosis of Edaravone After Experimental Intracerebral Hemorrhage.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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
9 citing papers in PubMed, 10 citations in OpenAlex.
- Edaravone Attenuates Retinal Ganglion Cell Ferroptosis Induced by Ischemia Reperfusion via Inhibiting the p38 MAPK/ATF3 Signaling Pathway.Molecular neurobiology · 2026Article
- The role of stem cells and their engineering strategies in the repair of nerve damage in intracerebral hemorrhage.Cell & bioscience · 2026Review
- Betaine Inhibits Ferroptosis After Intracerebral Hemorrhage by Activating the Nrf2/HO-1 Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Apigenin regulates CCR5/JAK1/STAT1/MMPs signaling to alleviate secondary brain injury after intracerebral hemorrhage and its enhanced delivery via targeted nanoparticles.Journal of nanobiotechnology · 2025Article
- BMSCs-derived exosomal AKAP12 alleviates neuronal cell ferroptosis by inhibiting the STAT3 and ERK signaling pathways in spinal cord injury.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Tungsten-based polyoxometalate nanoclusters as ferroptosis inhibitors modulating S100A8/A9-mediated iron metabolism pathway for managing intracerebral haemorrhage.Journal of nanobiotechnology · 2025Article
- Ferroptosis-associated pathological injury mechanisms and therapeutic strategies after intracerebral hemorrhage.Frontiers in neurology · 2025Review
- Annao Pingchong decoction attenuates oxidative stress and neuronal apoptosis following intracerebral hemorrhage via RAGE-NOX2/4 axis.Frontiers in neuroscience · 2024Article
- Edaravone administration and its potential association with a new clinical syndrome in cerebral infarction patients: Three case reports.World journal of clinical cases · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal ferroptosis plays an important role in secondary brain injuries after intracerebral hemorrhage (ICH). Edaravone (Eda) is a promising free radical scavenger that inhibits ferroptosis in neurological diseases. However, its protective effects and underlying mechanisms in ameliorating post-ICH ferroptosis remain unclear. We employed a network pharmacology approach to determine the core targets of Eda against ICH. Forty-two rats were subjected to successful striatal autologous whole blood injection (n=28) or sham operation (n=14). The 28 blood-injected rats were randomly assigned to either the Eda or vehicle group (n=14) for immediate administration and then for 3 consecutive days. Hemin-induced HT22 cells were used for in vitro studies. The effects of Eda in ICH on ferroptosis and the MEK/ERK pathway were investigated in vivo and in vitro. Network pharmacology-based analysis revealed that candidate targets of Eda-treated ICH might be related to ferroptosis; among which prostaglandin G/H synthase 2 (PTGS2) was a ferroptosis marker. In vivo experiments showed that Eda alleviated sensorimotor deficits and decreased PTGS2 expression (all p<0.05) after ICH. Eda rescued neuron pathological changes after ICH (increased NeuN
Indexed as
Identifiers
What 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.