ArticleOpen life sciences2024
Kaempferol regulates apoptosis and migration of neural stem cells to attenuate cerebral infarction by
Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Neuroprotective Mechanisms of Kaempferol in Experimental Ischemic Stroke: A Preclinical Systematic Review.Molecular neurobiology · 2025Pooled it
- Phytocompounds Targeting Signaling Pathways in Stroke: Preclinical and Clinical Insights into Therapeutic Mechanisms and Neurotoxicity.Molecular neurobiology · 2026Review
- O-GlcNAcylation of IGF2BP2 promotes angiogenesis after ischemic stroke by stabilizing PPP2CA in an m6A-dependent manner : O-GlcNAcylation of IGF2BP2 alleviates ischemic brain injury.Journal of translational medicine · 2026Article
- 2D nanomaterial-triggered ferroptosis in cancer therapy.Journal of nanobiotechnology · 2025Review
- Polyphenols as Wnt/β-catenin pathway modulators: A promising strategy in clinical neurodegeneration.Animal models and experimental medicine · 2025Review
- Kaempferol modulates Wnt/ β-catenin pathway to alleviate preeclampsia- induced changes and protect renal and ovarian histomorphology.Journal of molecular histology · 2024Article
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2 authors.
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Abstract
Ischemic stroke remains a major cause of disability and death. Kaempferol (Kae) is a neuroprotective flavonoid compound. Thus, this study aimed to explore the impact of Kae on cerebral infarction. We generated the middle cerebral artery occlusion (MCAO) mouse model to study the effects of Kae on infarction volume and neurological function. The oxygen and glucose deprivation (OGD)/reoxygenation (R) model of neural stem cells (NSCs) was established to study the effects of Kae on cell viability, migration, and apoptosis. Cell processes were assessed by cell counting kit-8, Transwell assay, flow cytometry, and TUNEL analysis. The molecular mechanism was assessed using the Western blot. The results indicated that Kae attenuated MCAO-induced cerebral infarction and neurological injury. Besides, Kae promoted cell viability and migration and inhibited apoptosis of OGD/R-treated NSCs. Moreover, OGD/R suppressed total
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