ArticleScientific reports2026
Epigallocatechin-3-gallate mitigates cerebral ischemia-reperfusion injury by promoting microglia toward M2 phenotype via Nrf2/HO-1 pathway.
Article in Scientific reports, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke remains the leading disease in terms of global disability and fatality rates. Cerebral ischemia-reperfusion injury (CIRI) and neuroinflammation induced by CIRI represents a challenge for clinical therapy of ischemic stroke. Epigallocatechin-3-gallate (EGCG), the predominant catechin in green tea, is known to mitigate ischemic stroke and inflammation, while its role in regulating neuroinflammation post-recanalization remains unclear. This study aimed to explore the effect and mechanism of EGCG on the regulation of CIRI. The CIRI in vivo model was established by middle cerebral artery occlusion/reperfusion (MCAO/R) in rats and EGCG was administered via intracerebroventricular injection before MCAO/R. The neurological scores, infarct volume, neuronal injury, and microglial biomarkers were evaluated. BV2 cells subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) were used to establish an in vitro CIRI model. After pretreatment with EGCG and/or ML385, OGD/R, cell viability, microglial biomarkers, pro-inflammatory and anti-inflammatory factors, and transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) were detected. Different conditioned media collected from BV2 cells were used for culturing the neuronal mimic cell line SH-SY5Y. EGCG administration in vivo significantly improved neurological deficits, infarct volume, and neuronal damage. Moreover, pretreatment with EGCG significantly increased BV2 cells viability and anti-inflammatory factors, and reduced toxicity and ferroptosis in SH-SY5Y cells. Furthermore, the upregulation of M2 markers was consistent with in vivo experiments. However, this protective effect was abolished by ML385, an Nrf2 inhibitor. EGCG upregulated Nrf2 and HO-1 protein expression, thus promoting microglial polarization toward the M2 phenotype. EGCG has a protective effect on CIRI by promoting the polarization of microglia toward the M2 phenotype via the Nrf2/HO-1 pathway to inhibit ferroptosis of neuron, which may provide a novel target for ischemic stroke treatment.
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.