ArticleInternational journal of medical sciences2022
Raddeanin A (RA) reduced acute inflammatory injury in mouse experimental cerebral hemorrhage by suppression of TLR4.
Article in International journal of medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- Development and validation of a machine learning-based predictive model for prognosis in cerebral hemorrhage patients after hyperbaric oxygen therapy.Medical gas research · 2027Article
- Sympathetic Overactivation Drives Neurogenic Alveolar Epithelial Pyroptosis via the PIEZO2-ER Stress Pathway in Acute Lung Injury Following Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2026Article
- A synergistic nanozyme platform breaking the neuroinflammatory-oxidative stress cycle for extended pain relief.International journal of pharmaceutics: X · 2026Article
- Raddeanin A (RA) Inhibited EMT and Stemness in Glioblastoma via downregulating Skp2.Journal of Cancer · 2025Article
- Raddeanin A Protects the BRB Through Inhibiting Inflammation and Apoptosis in the Retina of Alzheimer's Disease.Neurochemical research · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spontaneous intracerebral hemorrhage (ICH) is associated with high mortality and disability rates. The microglia-induced inflammatory response is a critical factor determining brain tissue damage after ICH. Raddeanin A (RA) is a natural triterpenoid compound with anti-inflammatory effects, although its effects on ICH and the underlying molecular mechanism have not been elucidated. In this study, we found that RA reduced the volume of cerebral hematoma and cerebral edema, attenuated neuronal apoptosis and improved the behavioral indices in a murine model of acute cerebral hemorrhage. Mechanistically, RA downregulated the TLR4-mediated pro-inflammatory effectors, reduced infiltration of microglia in peri-intracerebral hemorrhage and inhibited apoptosis of neurons co-cultured with activated microglia. In conclusion, RA can alleviate ICH-related tissue damage and promote the recovery of neuronal function by suppressing microglia-induced inflammation and apoptosis.
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Registered trials
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