ArticlePhytotherapy research : PTR2026
Luteolin Improves BBB Integrity Following Ischemic Stroke Injury by Downregulating the Expression of LRP1 and MMP9.
Article in Phytotherapy research : PTR, 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.
- Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders.Frontiers in pharmacology · 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
10 authors.
Funding
Abstract
Ischemic stroke is a prevalent neurological disorder often resulting in brain tissue injury and blood-brain barrier (BBB) damage. Luteolin (LUT), a natural polyphenolic compound in grape skin, wine, and other plants, has neuroprotective properties against ischemic stroke. However, it remains unclear whether its protective effect involves alterations in BBB integrity. This study aimed to examine the BBB-protective impact of LUT in a photothrombotic (PT) mouse model and oxygen-glucose deprivation (OGD) cell model and investigate its underlying mechanism. First, we used neurofunctional scoring, 2,3,5-triphenyltetrazolium chloride staining, Nissl staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) to evaluate the neuroprotective effects of LUT in ischemic stroke. Furthermore, we assessed the impact of LUT on BBB permeability using Evans Blue staining, brain water content, transendothelial electrical resistance, FITC, and flow cytometry techniques. We also examined the expression of tight junction (TJ) proteins related to BBB integrity using Western blotting. Finally, we validated the potential mechanism of action of LUT using short hairpin RNA (shRNA) technology. LUT alleviated the cerebral infarct area and neuronal apoptosis in the PT mouse model, reduced brain water content and Evans Blue leakage, decreased bEnd.3 cell apoptosis in the OGD model, increased transmembrane resistance, and reduced FITC leakage. LUT also counteracted the degradation of TJ proteins and decreased the expression of MMP9. Furthermore, the improvement was weakened when LRP1 was interfered with using shRNA. Our study suggests that LUT has the potential to improve BBB damage and exert neuroprotective effects following ischemic stroke. The mechanism of action may involve the inhibition of LRP1 and subsequent reduction in MMP9 expression.
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.