ArticleMetabolic brain disease2025
Genistein-3'-sodium sulfonate suppresses NLRP3-mediated cell pyroptosis after cerebral ischemia.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Therapeutic mechanisms of genistein in ischemic stroke: A systematic review of in vivo and in vitro studies.PloS one · 2025Pooled it
- BECN1 Protects Against Intestinal Ischemia/Reperfusion Injury by Promoting NLRP3 Ubiquitination and Suppressing Inflammasome Activation.Digestive diseases and sciences · 2026Article
- Genistein-3'-sodium sulfonate improves neuroinflammation, blood-brain barrier function, and microglial activation after chronic cerebral hypoperfusion by regulating TGR5.Metabolic brain disease · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Multidimensional targeting of ischemia-reperfusion injury by genistein: from molecular crosstalk to clinical translation.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
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Abstract
Cerebral ischemia-induced pyroptosis contributes to the dissemination of neuroinflammation, and Nod-like receptor protein-3 (NLRP3) inflammasome plays a key role in this process. Previous studies have indicated that Genistein-3'-sodiumsulfonate (GSS) can inhibit neuroinflammation caused by cerebral ischemia, exert cerebroprotective effects, but its specific mechanism has not been comprehensively understood. The aim of this study was to explore the effect of GSS on ischemic stroke-induced cell pyroptosis. SD rats were randomly assigned to Sham group, transient middle cerebral artery occlusion (tMCAO) group, and tMCAO + GSS group. The open field test (OFT) was utilized to assess animals' spontaneous movement and anxiety-like behavior. Immunofluorescence was adopted to observe nod-like receptor pyrin domain containing 3 (NLRP3)/neuronal nuclei (NeuN) double-positive cells in the ischemic penumbra of each group. Western blot (WB) was conducted to detect levels of NLRP3 inflammasomes and pyroptosis-related proteins in the ischemic cortex tissue. Furthermore, the G protein-coupled estrogen receptor 1 (GPER1) inhibitor G15 was administered to monitor tMCAO rats' motor function, emotional state, and NLRP3 inflammasome activation. Compared with the Sham group, rats in the tMCAO group exhibited significant motor dysfunction and anxiety, increased NLRP3
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