ArticleAmerican journal of translational research2018
3'-Daidzein sulfonate sodium provides neuroprotection by promoting the expression of the α7 nicotinic acetylcholine receptor and suppressing inflammatory responses in a rat model of focal cerebral ischemia.
Article in American journal of translational research, 2018. 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, 8 citations in OpenAlex.
- Genistein-3'-sodium sulfonate improves neuroinflammation, blood-brain barrier function, and microglial activation after chronic cerebral hypoperfusion by regulating TGR5.Metabolic brain disease · 2026Article
- 3'-Daidzein Sulfonate Sodium Protects against Glutamate-induced Neuronal Injuries by Regulating NMDA Receptors.Current pharmaceutical design · 2024Article
- Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review).International journal of molecular medicine · 2022Review
- CHRFAM7A Overexpression Attenuates Cerebral Ischemia-Reperfusion Injury via Inhibiting Microglia Pyroptosis Mediated by the NLRP3/Caspase-1 pathway.Inflammation · 2021Article
- Smoking cessation increases levels of osteocalcin and uncarboxylated osteocalcin in human sera.Scientific reports · 2020Observational
- 3'-Daidzein Sulfonate Sodium Protects Against Chronic Cerebral Hypoperfusion-Mediated Cognitive Impairment and Hippocampal Damage via Activity-Regulated Cytoskeleton-Associated Protein Upregulation.Frontiers in neuroscience · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a previous study using a rat model of focal cerebral ischemia/reperfusion (I/R) injury, we found that 3'-Daidzein sulfonate sodium (DSS), a derivative of daidzein, exerts neuroprotective effects by alleviating brain edema and reducing levels of interleukin (IL)-6. The present study was designed to further examine the potential mechanisms of the neuroprotective properties of DSS in a rat model of cerebral I/R injury. We found that treatment with DSS ameliorated neurological deficit, infarct size, and cerebral water content in rats with cerebral I/R injury. Moreover, treatment with DSS significantly reduced the levels of IL-1β, IL-6, and tumor necrosis factor (TNF)-α in serum and in the ischemic penumbra. Additionally, DSS treatment increased the expression of nicotinic acetylcholine receptor alpha 7 (α7nAChR), and inhibited the expression of glial fibrillary acidic protein, phosphorylated p65 nuclear factor κB, and phosphorylated inhibitor of NF-κBα, suggesting that DSS provides neuroprotection by suppressing inflammatory responses after focal cerebral I/R injury. Notably, α-bungarotoxin, an antagonist of α7nAChR, reversed the neuroprotective effects of DSS after cerebral I/R injury, suggesting that inhibition of α7nAChR expression is sufficient for reversal of the neuroprotective effects of DSS. In conclusion, we found that DSS treatment provides neuroprotection by promoting α7nAChR expression in a rat model of focal cerebral ischemia, thus establishing α7nAChR as a potential therapeutic target in cerebral I/R injury.
Indexed as
Identifiers
30662599PMC6291707W2991388147What OpenQuestion holds
Registered trials
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