ArticleMolecular neurobiology2023
Catalpol Alleviates Ischemic Stroke Through Promoting Angiogenesis and Facilitating Proliferation and Differentiation of Neural Stem Cells via the VEGF-A/KDR Pathway.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
- Canonical Wnt pathway mediates catalpol-induced epithelial differentiation of porcine metanephric mesenchymal cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- 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
- Catalpol: an natural multifunctional iridoid glycoside with promising therapeutic properties.Frontiers in molecular biosciences · 2026Review
- Research Hotspots and Frontiers of Ischemic Stroke and Traditional Chinese Medicine: A Knowledge Mapping and Text Mining Analysis.Current neuropharmacology · 2026Article
- Iridoids as Multi-target Neuroprotective Agents for Ischemic Stroke: Mechanisms and Therapeutic Potential.Mini reviews in medicinal chemistry · 2026Review
- Research Progress on the Multitarget Mechanisms of Terpenoids in the Treatment of Ischemic Stroke.Stroke research and treatment · 2026Review
- Catalpol: An Iridoid Glycoside With Potential in Combating Cancer Development and Progression-A Comprehensive Review.Phytotherapy research : PTR · 2025Review
- The Utilization Value of Condensate Water from the Drying Process ofMetabolites · 2025Article
- Therapeutic potential of natural products in ischemic stroke: targeting angiogenesis.Frontiers in pharmacology · 2025Review
- Pharmacological effects and mechanisms of medicine food homology species and active ingredients in ameliorating ovarian aging.Frontiers in nutrition · 2025Review
- Hypoxia-inducible Factor-1α Pathway in Cerebral Ischemia: From Molecular Mechanisms to Therapeutic Targets.CNS & neurological disorders drug targets · 2025Review
- Catalpol regulates apoptosis and proliferation of endothelial cell via activating HIF-1α/VEGF signaling pathway.Scientific reports · 2024Article
- Transcriptional Differential Analysis of Nitazoxanide-Mediated Anticanine Parvovirus Effect in F81 Cells.Viruses · 2024Article
- Catalpol promotes hippocampal neurogenesis and synaptogenesis in rats after multiple cerebral infarctions by mitochondrial regulation: involvement of the Shh signaling pathway.Frontiers in pharmacology · 2024Article
- Rehmanniae Radix Preparata ameliorates behavioral deficits and hippocampal neurodevelopmental abnormalities in ADHD rat model.Frontiers in neuroscience · 2024Article
- Fullerenols Ameliorate Social Deficiency and Rescue Cognitive Dysfunction of BTBR TInternational journal of nanomedicine · 2024Article
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8 authors at 2 institutions in 1 country.
Funding
Abstract
Stroke is one of the leading causes of disability and death globally with a lack of effective therapeutic strategies. Catalpol is a bioactive compound derived from the traditional Chinese medicine Rehmannia glutinosa and it has been shown to be protective against various neurological diseases. The potential roles of catalpol against ischemic stroke are still not completely clear. In this study, we examined the effect and mechanism of catalpol against ischemic stroke using in vivo rat distal middle cerebral artery occlusion (dMCAO) and in vitro oxygen-glucose deprivation (OGD) models. We demonstrated that catalpol indeed attenuated the neurological deficits caused by dMCAO and improved neurological function. Catalpol remarkably promoted angiogenesis, promoted proliferation and differentiation of neural stem cells (NSCs) in the subventricular zone (SVZ), and prevented neuronal loss and astrocyte activation in the ischemic cortex or hippocampal dentate gyrus (DG) in vivo. The vascular endothelial growth factor receptor 2 (KDR, VEGFR-2) inhibitor SU5416 and VEGF-A shRNA were used to investigate the underlying mechanisms. The results showed that SU5416 administration or VEGF-A-shRNA transfection both attenuated the effects of catalpol. We also found that catalpol promoted the proliferation of cultured brain microvascular endothelial cells (BMECs) and the proliferation and differentiation of NSCs subjected to OGD insult in vitro. Interestingly, the impact of catalpol on cultured cells was also inhibited by SU5416. Moreover, catalpol was shown to protect NSCs against OGD indirectly by promoting BMEC proliferation in the co-cultured system. Taken together, catalpol showed therapeutic potential in cerebral ischemia by promoting angiogenesis and NSC proliferation and differentiation. The protective effects of catalpol were mediated through VEGF-A/KDR pathway activation.
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