ArticlePharmaceutics2022
Isosteviol Sodium (STVNA) Reduces Pro-Inflammatory Cytokine IL-6 and GM-CSF in an In Vitro Murine Stroke Model of the Blood-Brain Barrier (BBB).
Article in Pharmaceutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Alterations in the DTI-ALPS index and choroid plexus volume are associated with symptom severity in children with tic disorders.BMC neurology · 2026Article
- Hydroxychloroquine Prevents High-altitude Cerebral Edema by Inhibiting Endothelial Claudin-5 Autophagic Degradation.Current neuropharmacology · 2026Article
- Isosteviol Sodium Promotes Neurological Function Recovery in a Model of Spinal Cord Injury in Rats.Immunity, inflammation and disease · 2025Article
- Relationship between neuroinflammatory markers in plasma and cerebrospinal fluid before and after hip arthroplasty and postoperative delirium.American journal of translational research · 2025Article
- MicroRNA-199a-5p attenuates blood-brain barrier disruption following ischemic stroke by regulating PI3K/Akt signaling pathway.PloS one · 2024Article
- High-throughput drug screening to investigate blood-brain barrier permeabilityFrontiers in drug delivery · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Early treatment with glucocorticoids could help reduce both cytotoxic and vasogenic edema, leading to improved clinical outcome after stroke. In our previous study, isosteviol sodium (STVNA) demonstrated neuroprotective effects in an in vitro stroke model, which utilizes oxygen-glucose deprivation (OGD). Herein, we tested the hypothesis that STVNA can activate glucocorticoid receptor (GR) transcriptional activity in brain microvascular endothelial cells (BMECs) as previously published for T cells. STVNA exhibited no effects on transcriptional activation of the glucocorticoid receptor, contrary to previous reports in Jurkat cells. However, similar to dexamethasone, STVNA inhibited inflammatory marker IL-6 as well as granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion. Based on these results, STVNA proves to be beneficial as a possible prevention and treatment modality for brain ischemia-reperfusion injury-induced blood-brain barrier (BBB) dysfunction.
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Registered trials
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