ArticleCNS neuroscience & therapeutics2025
Investigation of Anti-Apoptotic Effects and Mechanisms of Astragaloside IV in a Rat Model of Cerebral Ischemia-Reperfusion Injury.
Article in CNS neuroscience & therapeutics, 2025. 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.
- Multi-omics analysis of untargeted metabolomics and gut microbiota study on the mechanism of Astragalus-Safflower to coordinate the regulation of energy metabolism pathways and gut microbiota remodeling to improve ischemic stroke.Metabolic brain disease · 2026Article
- Article
- Astragaloside IV suppresses neuroinflammation via PI3K/Akt/NF-κB to ameliorate cerebral ischemia-reperfusion injury based on network pharmacology analysis and experimental validation.Frontiers in immunology · 2026Article
- Qishiwei Zhenzhu Pills Protect Against Cerebral Ischemia via the P53/Cytochrome C/Apoptotic Protease Activating Factor 1-Mediated Mitochondrial Apoptosis Pathway.CNS neuroscience & therapeutics · 2025Article
- Therapeutic potential of natural products in ischemic stroke: targeting angiogenesis.Frontiers in pharmacology · 2025Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Astragaloside IV is a potential natural neuroprotective agent for stroke: a review.Frontiers in pharmacology · 2025Review
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Authors and funding
11 authors.
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Abstract
backgroundIschemic stroke is a prevalent and life-threatening cerebrovascular disease that is challenging to treat and associated with a poor prognosis. Astragaloside IV (AS-IV), a primary bioactive component of Astragali radix, has demonstrated neuroprotective benefits in previous studies. This study aimed to explore the mechanisms through which AS-IV may treat cerebral ischemia-reperfusion injury (CIRI).
methodsNetwork pharmacology was employed to identify key targets and pathways of AS-IV in CIRI therapy, combined with molecular docking to predict binding affinity. Male Sprague-Dawley rats were randomly assigned to sham, MCAO/R, AS-IV, SP600125 (JNK inhibitor), AS-IV + SP600125, and 3-n-Butylphthalide (NBP) groups. Neurobehavioral deficits were assessed, and brain tissue damage was visualized through 2,3,5-triphenyltetrazolium chloride, H&E, and TUNEL staining. Immunohistochemistry was employed to detect CytC- and caspase-3-positive cells, while Western blotting, qPCR, and ELISAs were used to analyze apoptosis-related markers.
resultsA total of 48 key targets of AS-IV predicted to be involved in the treatment of CIRI were identified, enriched in 136 pathways. AS-IV was effectively bound to the top five targets from 48 targets, and those associated with the c-Jun N-terminal kinase (JNK)/Bid pathway, with binding energy values below -5.0 kJ·mol
conclusionAS-IV may suppress apoptosis partly through the modulation of JNK/Bid signaling, exerting neuroprotective effects. These findings support the potential development of AS-IV-based therapies for stroke treatment.
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