ArticleNeuroreport2025
Resveratrol-mediated NRF2/HO-1 signaling pathway to improve postoperative cognitive dysfunction in elderly rats.
Article in Neuroreport, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- Adenosine APharmaceuticals (Basel, Switzerland) · 2026Article
- PLCG1 promotes sevoflurane-induced neuronal ferroptosis by enhancing K63-linked ubiquitination and proteasomal degradation of LAMP2A.Experimental brain research · 2026Article
- Ferroptosis: an emerging key mechanism linking aging, surgical and anesthetic exposure to postoperative cognitive dysfunction.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
To investigate the effects of resveratrol (RES) on cognitive function and its modulation of the NRF2/HO-1 signaling pathway in a rodent model of postoperative cognitive dysfunction (POCD). A POCD model was established in aged Sprague-Dawley rats using sevoflurane anesthesia and laparotomy. Rats were divided into four groups: control, POCD, RES, and POCD + RES. Cognitive performance was assessed using the Morris water maze. Hippocampal tissues were analyzed for neuronal condition using hematoxylin and eosin and Nissl staining. The expression levels of inflammatory cytokines and oxidative stress markers were quantified by enzyme-linked immunosorbent assay. The messenger RNA and protein levels of NRF2, KEAP1, HO-1, and SOD2 were measured using real-time quantitative polymerase chain reaction and western blotting. RES treatment improved cognitive function, as evidenced by reduced escape latency and increased platform crossings in the Morris water maze. Histopathological analysis showed restoration of hippocampal structure and increased neuronal viability. RES significantly reduced proinflammatory cytokines interleukin (IL)-1 and IL-6 while increasing IL-10 levels. In addition, RES activated the NRF2/HO-1 pathway by upregulating NRF2, HO-1, and SOD2 expression while downregulating KEAP1. RES mitigates cognitive deficits in POCD by reducing neuroinflammation and oxidative stress through activation of the NRF2/HO-1 signaling pathway. These findings suggest RES is a potential therapeutic candidate for the treatment of POCD in elderly patients.
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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.