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Mdivi-1 Mediates Apoptotic Protein Bax Insertion Activation and Cytochrome C Release on Oxygen and Glucose Deprived Cortical Neurons

CUI Mei;YANG Qi;DONG Qiang;Department of Neurology,Huashan Hospital,Fudan University;  
Objective:To study the effect of mitochondrial fission protein inhibitor Mdivi-1 on apoptotic protein Bax activation insertion and cytochrome C release of oxygen and glucose deprived cortical neurons. Methods: Primary cultured cortical neurons were treated with different doses of Mdivi-1 after oxygen-glucose deprivation procedure. MTT was used to evaluate the cell viability. After OGD treatment the neurons were treated with 10 μmol/L Mdivi-1, co-immunoprecipitation or alkali treatment were used to determine Bax activation and insertion. Mitochondrial and cytosolic fraction proteins were extracted, Western Blot was used to detect the cytochrome C release. Results: Mdivi-1 significantly improved cell viability in a dose-dependent manner. Mdivi-1 blocked apoptotic protein Bax insertion and activation and subsequent cytochrome C release induced by OGD. Conclusion: Mitochondrial fission protein inhibitor Mdivi-1 has a neuroprotective effect on neurons after OGD, probably mediated by anti-apoptotic effects.
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