ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2023
Dihydromyricetin Alleviates Ischemic Brain Injury by Antagonizing Pyroptosis in Rats.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Identification of NETs-related genes as diagnostic biomarkers in ischemic stroke using RNA sequencing and single-cell analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Pharmacological mechanisms and potential clinical applications of Dihydromyricetin in neurological disorders.Frontiers in pharmacology · 2025Review
- Therapeutic potential of combination medicinal mushrooms (NevG) in ischemic stroke: correlating motor function, cognitive recovery, and hippocampal integrity in MCAO rats.Frontiers in pharmacology · 2025Article
- Dihydromyricetin: an emerging compound with comprehensive effects on multiple systems.Frontiers in pharmacology · 2024Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemic stroke is a worldwide disease that seriously threatens human health, and there are few effective drugs to treat it. Dihydromyricetin (DHM) has anti-inflammatory, antioxidant, and antiapoptotic functions. We identified pyroptosis following ischemic stroke. Here, we investigated the effect of DHM on ischemic stroke and pyroptosis. In the first part of the experiment, Sprague-Dawley rats were randomly divided into the sham group and MCAO group. The MCAO model was established by occlusion of the middle cerebral artery for 90 min using a silica gel suture. The ischemic penumbra was used for mRNA sequencing 1 day after reperfusion. In the second part, rats were divided into the sham group, MCAO group, and DHM group. DHM was injected intraperitoneally at the same time as reperfusion starting 90 min after embolization for 7 consecutive days. The changes in pyroptosis were observed by morphological and molecular methods. The transcriptomics results suggested the presence of NLRP3-mediated pyroptotic death pathway activation after modeling. The Longa score was increased after MCAO and decreased after DHM treatment. 2,3,5-Triphenyltetrazolium chloride (TTC) staining showed that DHM could reduce the infarct volume induced by MCAO. Nissl staining showed disordered neuronal arrangement and few Nissl bodies in the MCAO group, but this effect was reversed by DHM treatment. Analysis of pyroptosis-related molecules showed that the MCAO group had serious pyroptosis, and DHM effectively reduced pyroptosis. Our results demonstrate that DHM has a neuroprotective effect on ischemic stroke that is at least partly achieved by reducing pyroptosis.
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Registered trials
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