Title:3′-Daidzein Sulfonate Sodium Protects against Glutamate-induced Neuronal
Injuries by Regulating NMDA Receptors
Volume: 30
Issue: 22
Author(s): Ruixue Feng, Li Luo, Zun Han, Yue Qi, Hai Xiao, Cheng Huang, Weijie Peng, Ruizhen Liu*Zhihua Huang*
Affiliation:
- Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education, Gannan
Medical University, Ganzhou 341000, China
- Ganzhou Key Laboratory of Neuroinflammation Research, Gannan Medical University, Ganzhou 341000, China
- School of Basic Medical Sciences, Gannan Medical University, Ganzhou 341000, China
- Key Laboratory of Prevention and Treatment of Cardiovascular and Cerebrovascular Diseases of Ministry of Education, Gannan
Medical University, Ganzhou 341000, China
- Ganzhou Key Laboratory of Neuroinflammation Research, Gannan Medical University, Ganzhou 341000, China
- School of Basic Medical Sciences, Gannan Medical University, Ganzhou 341000, China
Keywords:
Excitotoxicity, 3′-Daidzein sulfonate sodium, neuroprotection, NMDA receptors, molecular mechanisms, neuronal injuries.
Abstract:
Background: It was previously found that 3'-Daidzein Sulfonate Sodium (DSS) exhibits protective
effects on cerebral ischemia/reperfusion injury (CI/RI).
Aim: This study aimed to explore the underlying molecular mechanisms involved in the neuroprotective effects
of DSS against ischemic stroke.
Methods: In this study, rats with transient middle cerebral artery occlusion (tMCAO) were used as an in vivo
model, whereas PC12 cells treated with glutamate alone and rat primary cortical neurons treated with the combination
of glutamate and glycine were used as in vitro models. Cell viability and lactate dehydrogenase (LDH)
release were used to evaluate cell injury. Cell apoptosis was determined by flow cytometry. Quantitative polymerase
chain reaction (qPCR), Western blotting, and immunofluorescent staining methods were used to determine
the mRNA expressions and protein levels and location.
Results: It was found that DSS significantly suppressed the impaired viability of PC12 cells induced by glutamate.
DSS also increased cell viability while reducing the LDH release and apoptosis in primary cortical neurons
injured by glutamate and glycine. In addition, DSS decreased GluN2B subunit expression while enhancing
the expressions of GluN2A subunit and PSD95 in tMCAO rats’ brains.
Conclusion: This study demonstrated that DSS protects against excitotoxic damage in neurons induced by
CI/RI through regulating the expression of NMDA receptors and PSD95. Our findings provide experimental
evidence for the potential clinical administration of DSS in ischemic stroke.