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Resveratrol Alleviates Ischemia-Reperfusion-Induced Neuronal Damage by Inhibiting NR3C2-Mediated TRIM28 Expression
Yan Li1, Haiwei Xie1, Shuang Liu1
1Department of Anesthesiology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, 421002 Hengyang, Hunan, China.
Journal of Integrative Neuroscience
|April 30, 2025
Summary
Resveratrol (Res) treatment alleviates cerebral ischemia-reperfusion injury (CIRI) by inhibiting nuclear receptor subfamily 3 group C member 2 (NR3C2) and tripartite motif containing 28 (TRIM28). This neuroprotective effect balances apoptosis and autophagy, offering new therapeutic strategies for CIRI.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Cerebral ischemia-reperfusion injury (CIRI) causes neuronal damage via apoptosis and autophagy dysregulation.
- Resveratrol (Res), a natural polyphenol, exhibits neuroprotective properties against CIRI.
- This study explores Res's role in modulating NR3C2 and TRIM28 to balance apoptosis and autophagy in CIRI.
Purpose of the Study:
- To investigate the therapeutic effects of Resveratrol on cerebral ischemia-reperfusion injury (CIRI).
- To elucidate the underlying mechanisms involving NR3C2 and TRIM28 in Res's neuroprotection.
- To determine how Res balances apoptosis and autophagy in CIRI models.
Main Methods:
- In vivo studies utilized MCAO/R rat models to assess cognitive function, infarct volume, and inflammatory markers.
- In vitro experiments used OGD/R-treated PC12 cells to evaluate cell viability, apoptosis, and autophagy.
- Gene expression (RT-qPCR, WB) and protein interactions (dual luciferase, ChIP-qPCR) were analyzed for NR3C2 and TRIM28.
Main Results:
- Res treatment improved cognitive performance and reduced infarct size in rats.
- Res enhanced cell viability, reduced apoptosis, and restored autophagy balance in OGD/R-treated cells.
- NR3C2 was found to directly regulate TRIM28 transcription, mediating Res's neuroprotective effects.
Conclusions:
- Resveratrol inhibits NR3C2 expression, which subsequently regulates TRIM28 transcription.
- This NR3C2-TRIM28 pathway modulation by Res alleviates CIRI-induced apoptosis and autophagy dysregulation.
- The findings highlight NR3C2 and TRIM28 as potential therapeutic targets for CIRI treatment.
