ArticleScientific reports2026
Pramipexole alleviates ferroptosis in HT22 cells induced by oxygen-glucose deprivation/reoxygenation via the Nrf2/SLC7A11/GPX4 pathway.
Article in Scientific reports, 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.
- Total Astragalus Saponins Modulate Ferroptosis Pathways in Cigarette Smoke and LPS-Induced Models of COPD: An in vitro and in vivo Investigation.Journal of inflammation research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Pramipexole, a dopamine receptor agonist, is clinically employed in the treatment of Parkinson's disease. Accumulating evidence has demonstrated that it can enhance neurological function following cerebral ischemia-reperfusion via multiple mechanisms. This study is designed to explore whether pramipexole exerts a protective effect on neurons subjected to oxygen-glucose deprivation/reperfusion by inhibiting the ferroptosis pathway. Firstly, CCK8 assay was employed to evaluate cell viability to determine the optimal intervention time and dosage during oxygen-glucose deprivation/reperfusion injury. Mitochondrial function was evaluated via transmission electron microscopy and JC-1 fluorescent probe. Intracellular iron, glutathione, and glutathione peroxidase 4 enzyme activity were measured using ELISA. Ferroptosis-related proteins and genes were analyzed by immunofluorescence, real-time qPCR, and western blot. And then, a ferroptosis inducer (Erastin) was used as a positive control to validate the link between pramipexole's effects and ferroptosis regulation. Oxygen-glucose deprivation/reperfusion exposure reduced cell viability, impaired mitochondrial membrane potential, elevated intracellular iron and reactive oxygen species, and suppressed antioxidant capacity. Pramipexole treatment reversed these pathological changes and activated the nuclear factor E2-related factor 2/solute carrier family 7 member 11/glutathione peroxidase 4 signaling axis. Erastin recapitulated oxygen-glucose deprivation/reperfusion-induced cellular dysfunction, which was also mitigated by pramipexole. Pramipexole alleviates oxygen-glucose deprivation/reperfusion-induced neuronal damage and oxidative stress by activating the nuclear factor E2-related factor 2/solute carrier family 7 member 11/glutathione peroxidase 4 pathway to inhibit ferroptosis, highlighting its potential as a therapeutic agent for cerebral ischemia-reperfusion injury.
Indexed as
Identifiers
What Socratic 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 Socratic graph.