Salvianolic Acid B Attenuates Excitotoxic Neuronal Injury After Transient Cerebral Ischemia

BACKGROUND/AIM: models of ischemic injury to investigate whether Sal B attenuated excitotoxic neuronal damage. MATERIALS AND METHODS: ) to induce hypoxia-like injury, after which neuronal viability and apoptotic markers were evaluated. A middle cerebral artery occlusion (MCAO) rat model was constructed to examine the ischemia-induced alterations in excitatory neurotransmission-related proteins. Protein expression was analyzed using western blotting and immunofluorescence, while gene expression was assessed using quantitative real-time PCR. RESULTS: -induced apoptotic signaling, as indicated by the decreased cleavage of caspase-3 and PARP-1. In the MCAO model, ischemia altered the expression of glutamatergic markers, including glutamate receptor-1 (GluA1), vesicular glutamate transporter-2 (VGLUT2), and N-methyl-D-aspartate receptor-1 (NMDAR1). Sal-B treatment attenuated these alterations, reducing the GluA1 and VGLUT2 intensities in NeuN-positive cortical neurons. Furthermore, Sal B decreased mRNA expression of the hypoxia marker HIF1α and the pro-apoptotic factor Noxa, while increasing expression of the anti-apoptotic Bcl2 family members, Bcl-2 and Bcl-xL. CONCLUSION: SalB 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.