ArticleJournal of inflammation research2026
NRG1 Suppresses NLRP3 Inflammasome Activation and Endothelial-Mesenchymal Transition in Cerebral Ischemia-Reperfusion Injury: Association with the AKT/NF-κB Pathway.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- Review
- Association of peripheral NLRP3 inflammasome activation with prevalent and incident chronic kidney disease in patients with obstructive sleep apnea: a prospective study.Sleep & breathing = Schlaf & Atmung · 2026Observational
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Endothelial damage and NLRP3 inflammasome activation are key mechanisms underlying cerebral ischemia-reperfusion (I/R) injury. Neuregulin-1 (NRG1) alleviates endothelial damage, blood-brain barrier (BBB) disruption, and neurological deficits following acute ischemic stroke (AIS). This study investigates whether NRG1 attenuates endothelial-mesenchymal transition (EndMT) during endothelial injury by suppressing NLRP3 inflammasome activation, potentially through the AKT/NF-κB pathway, in cerebral I/R injury. Methods: Middle cerebral artery occlusion/reperfusion (MCAO/R) mouse models and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated immortalized human cerebral microvascular endothelial cells (hCMEC/D3) were established and treated with NRG1. Neurological deficits were assessed using the modified Neurological Severity Score (mNSS), while cerebral infarct volume and caspase-1 activity were quantified. Cell viability and death were evaluated by the Cell Counting Kit-8 (CCK-8), lactate dehydrogenase (LDH) assays, and TUNEL staining. Protein expression was analyzed using Western blotting and immunofluorescence staining. Results: NRG1 intervention significantly improved mNSS, reduced cerebral infarct volume, and decreased caspase-1 activity in MCAO/R mice. In OGD/R-treated hCMEC/D3, NRG1 enhanced cell viability while reducing cell death, as indicated by decreased LDH release and TUNEL-positive cells. Western blotting and immunofluorescence staining revealed that NRG1 enhanced AKT phosphorylation, inhibited NF-κB p65 phosphorylation, and downregulated NLRP3 and IL-1β expression. These effects were associated with the amelioration of occludin reduction and suppression of α-smooth muscle actin (α-SMA) increase during EndMT progression. Conclusion: The results demonstrate that NRG1 reduces cerebral infarct volume, alleviates neurological deficits, and suppresses NLRP3 inflammasome activation in association with modulation of the AKT/NF-κB pathway, thereby attenuating EndMT-associated proteins following cerebral I/R injury.
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