ArticleIn vivo (Athens, Greece)
Salvianolic Acid B Attenuates Excitotoxic Neuronal Injury After Transient Cerebral Ischemia.
Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND/
aimExcitotoxic neuronal injury plays a central role in the pathological cascade which follows cerebral ischemia. Excessive glutamatergic signaling leads to calcium overload and the activation of apoptotic pathways, ultimately triggering neuronal death. Salvianolic acid B (Sal B), a water-soluble polyphenolic compound derived from MATERIALS AND
methodsPrimary cortical neurons were exposed to cobalt chloride (CoCl
resultsSal B significantly improved neuronal viability and reduced CoCl
conclusionSalB attenuates hypoxia- and ischemia-induced neuronal injury and modulates excitatory neurotransmission in the ischemic cortex. These findings indicate that Sal B exerts neuroprotective effects partly through the regulation of excitatory synaptic signaling following cerebral ischemia.
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