ArticleTranslational neuroscience2020
Saikosaponin A attenuates neural injury caused by ischemia/reperfusion.
Article in Translational neuroscience, 2020. 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, 17 citations in OpenAlex.
- Saikosaponin A, a bioactive compound from Bupleuri radix, protects dopaminergic neurons and correlates with NURR1 expression in 6-hydroxydopamine-injected hemi-Parkinsonian mouse model.Pharmacological reports : PR · 2026Article
- Investigating the Mechanism of Yiqi Huoxue Jieyu Granules Against Ischemic Stroke Through Network Pharmacology, Molecular Docking and Experimental Verification.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring the Therapeutic Potential ofPharmaceuticals (Basel, Switzerland) · 2025Review
- Pharmacology, medical uses, and clinical translational challenges of Saikosaponin A: A review.Heliyon · 2024Review
- Saikosaponin A protects against uremic toxin indole‑3 acetic acid‑induced damage to the myocardium.Molecular medicine reports · 2023Article
- Role of traditional Chinese medicine monomers in cerebral ischemia/reperfusion injury:a review of the mechanism.Frontiers in pharmacology · 2023Review
- HMGB1 in nervous system diseases: A common biomarker and potential therapeutic target.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammation is involved in cerebral ischemia/reperfusion (I/R)-induced neurological damage. Saikosaponin A (SSa), extracted from
methodsRat middle cerebral artery occlusion (MCAO) model was employed in this study, and the cognitive and motor functions were detected by behavioral tests. Inflammatory cytokines in the serum were detected by ELISA kits. The expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and high-mobility group box 1 (HMGB1) in the brain tissues were assayed with Western blot.
resultsOur results showed that SSa pretreatment could significantly reduce brain damage, improve neurological function recovery, and decrease the water content of brain tissues when compared with the model group. SSa pretreatment significantly reduced the serum HMGB1 level and downregulated the contents of inflammatory cytokines including tumor necrosis factor-α, interleukin-1 beta, and interleukin-6. Furthermore, SSa pretreatment could attenuate the decreased TLR4 and nucleus NF-κB in the brain of MCAO rats. The protein level of HMGB1 in the nucleus was significantly upregulated in the SSa pretreatment group.
conclusionOur results suggested that the pretreatment with SSa provided significant protection against cerebral I/R injury in rats via its anti-inflammation property by inhibiting the nucleus HMGB1 release.
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