Authors
Mahrokh Janmohamadi, Amirreza Peyrovinasab, Arash Sarveazad, Niyousha Rahimimovaghar, Vafa Rahimi-Movaghar, Mahmoud Yousefifard
Published in
Brain injury. Pages 1-13. Aug 17, 2026. Epub Aug 17, 2026.
Abstract
Oxidative stress, inflammation, and apoptosis following traumatic brain injury (TBI) cause secondary damage that leads to long-term neurological impairments. Though its effectiveness in TBI remains largely underexplored, the natural polyphenol resveratrol (RES) shows neuroprotective effects. This meta-analysis assesses RES's therapeutic potential in rodent TBI models.
Medline, Embase, Scopus, and Web of Science (up to April 2025) were searched for studies evaluating RES in rodent TBI using PRISMA recommendations. Inclusion criteria were satisfied by 10 studies. Outcomes included cerebral edema, autophagy, inflammation, apoptosis, neuronal density, and neurological status. With 95% confidence intervals, random-effects models computed standardized mean differences. We looked at publication bias (Egger's test) and heterogeneity (I2).
RES notably lowered autophagy markers (Beclin-1; LC3II) and cerebral edema. It decreased apoptosis (caspase-3) and inflammation (IL-1β; TNF-α). In CA1 and CA3 areas, hippocampal neuron density increased. With lower escape latency in the Morris water maze and Neurological Severity Score, memory and neurological status improved.
By reducing edema, inflammation, and apoptosis, RES shows strong neuroprotection in rodent TBI models while maintaining neurons and improving recovery. RES is a reasonable contender for supplementary TBI treatment.
PMID:
42606086
Bibliographic data and abstract were imported from PubMed on 17 Aug 2026.
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