ArticleCNS neuroscience & therapeutics2026
Toosendanin Alleviates Cerebral Ischemia/Reperfusion Injury via Inhibiting Neural Ferroptosis Through Lipid Metabolic Reprogramming in MCAO Mice.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- HIF-1α in ischemic stroke: context-dependent roles in ferroptosis and neurovascular repair.Frontiers in neurology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundThe crosstalk between ferroptosis and neuroinflammation plays an important role in the pathogenesis of cerebral ischemia-reperfusion injury. Toosendanin (TSN), a triterpenoid compound, exhibits a wide range of pharmacological activities in human diseases. Here we investigated the potential neuroprotective effects of TSN in cerebral ischemia-reperfusion injury.
methodsIn our study, in vivo murine middle cerebral artery occlusion (MCAO) model and in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model were constructed to mimic cerebral ischemia-reperfusion injury. TTC staining, open-field test, Morris water maze test, hanging wire test, rotarod test, foot-fault test, hematoxylin and eosin (H&E) staining, flow cytometry, western blot and reverse transcription-quantitative PCR were conducted to evaluate the potential influence of TSN in cerebral ischemia-reperfusion injury.
resultsOur results indicated that post-stroke administration of TSN significantly reduced infarct volume and improved long-term functional recovery of MCAO mice. Mechanistically, TSN alleviated neural oxidative stress, lipid peroxidation, and ferroptosis in MCAO mice or in vitro after OGD/R. In addition, TSN modulated the infiltrating of immune cells in MCAO mice in vivo and T cell differentiation in vitro. Mechanistically, TSN directly interacted with ACSL4 and suppressed its enzymatic activity, thus suppressing the ACSL4/LPCAT3 axis to reduce the incorporation of pro-ferroptotic polyunsaturated fatty acids (PUFA) into phospholipids, and finally inhibiting lipid peroxidation and neural ferroptosis. In addition, the induction of ferroptosis abrogated the influence of TSN on immune infiltration and lipid metabolism in MCAO mice.
conclusionOur findings identify TSN as a promising therapeutic agent for cerebral ischemia-reperfusion injury via inhibiting ACSL4-mediated ferroptosis.
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.