Journal
CHINESE JOURNAL OF PHYSIOLOGY
Volume 58, Issue 4, Pages 244-253Publisher
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.4077/CJP.2015.BAD296
Keywords
apoptosis; Bc1-2 family; CoCl2; ERK1/2; MgSO4; mitochondria
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Funding
- Taiwan Department of Health Clinical Trial and Research Center of Excellence [DOH101-TD-B-111-004]
- Central Taiwan University of Science and Technology [CTU98-P-19, CTU100-P-08]
- China Medical University [CMU99-S-01, CMU96-272]
- Asia University
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Magnesium sulfate (MgSO4) ameliorates hypoxia/ischemia-induced neuronal apoptosis in a rat model. This study aimed to investigate the mechanisms governing the anti-apoptotic effect of MgSO4 on cobalt chloride (CoCl2)-exposed NB41A3 mouse neuroblastoma cells. MgSO4 increased the viability of NB41A3 cells treated with CoCl2 in a dose-dependent manner. MgSO4 treatment was shown to lead to an increase in the anti-apoptotic Bcl-2 family proteins, with a concomitant decrease in the pro-apoptotic proteins. MgSO4 also attenuated the CoCl2-induced disruption of mitochondrial membrane potential (Delta Psi(m)) and reduced the release of cytochrome c form the mitochondria to the cytosol. Furthermore, exposure to CoCl2 caused activation of the hypoxia-inducible factor la (HIF-1 alpha). On the other hand, MgSO4 markedly reduced CoCl2-induced HIF-l alpha activation and suppressed HIF-la downstream protein BNIP3. MgSO4 treatment induced ERK1/2 activation and attenuated CoCl2-induced activation of p38 and JNK. Addition of the ERK1/2 inhibitor U0126 significantly reduced the ability of MgSO4 to protect neurons from CoCl2-induced mitochondrial apoptotic events. However, incubation of cultures with the p38 and JNK inhibitors did not significantly affect MgSO4-mediated neuroprotection. MgSO4 appears to suppress CoCl2-induced NB41A3 cell death by activating ERK1/2/ MAPK pathways, which further modulates the role of Bcl-2 family proteins and mitochondria in NB41A3 cells. Our data suggest that MgSO4 may act as a survival factor that preserves mitochondrial integrity and inhibits apoptotic pathways.
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