ArticleTranslational neuroscience2020
EGCG treats ICH via up-regulating miR-137-3p and inhibiting Parthanatos.
Article in Translational neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Increasing Life Expectancy with Plant Polyphenols: Lessons from the Mediterranean and Japanese Diets.Molecules (Basel, Switzerland) · 2025Review
- Epigallocatechin gallate mitigates the motor deficits in a rotenone-induced Parkinson's disease rat model via promoting protein kinase D1 and inhibiting neuronal Parthanatos.Translational neuroscience · 2025Article
- Study on the Therapeutic Effects of Bisdemethoxycurcumin on a Cerebral Amyloid Angiopathy Mouse Model Established via Chronic Treatment With Five Vascular Risk Factors.Brain and behavior · 2025Article
- Dysregulation of Serum MicroRNA after Intracerebral Hemorrhage in Aged Mice.Biomedicines · 2023Article
- Treatment of radiation-induced brain injury with bisdemethoxycurcumin.Neural regeneration research · 2023Article
- EGCG promotes the sensory function recovery in rats after dorsal root crush injury by upregulating KAT6A and inhibiting pyroptosis.Translational neuroscience · 2023Article
- Artemisinin upregulates neural cell adhesion molecule L1 to attenuate neurological deficits after intracerebral hemorrhage in mice.Brain and behavior · 2022Article
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Authors and funding
13 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (-)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos.
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