Abstract：
:It has been well established that the mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) opener, diazoxide, has protective effects on the heart and brain following ischemia/reperfusion injury. However, the mechanism of the neuroprotective effects of diazoxide remains unclear. This study highlights the anti-apoptotic effects of the drug, which are mediated by specific regulation of apoptosis-inducing factor (AIF) in the process of oxygen and glucose deprivation (OGD)-induced apoptosis in SH-SY5Y cells. Our data showed that pretreatment with diazoxide in SH-SY5Y cells following OGD concentration-dependently increased cell viability. Compared to cells induced by OGD alone, cells pretreated with diazoxide displayed reduced rates of apoptosis, increased mitochondrial transmembrane potential (ΔΨm), and reduced AIF translocation to the cell nucleus. The protective effects of preconditioning with diazoxide were attenuated by 5-hydroxydecanoic acid (5-HD), a selective mitoK(ATP) channel antagonist. Meanwhile, cell death was blocked in OGD-induced cells stably transfected with the AIF-shRNA plasmid, and down-regulation of AIF reduced the diazoxide-mediated prevention of cell apoptosis as well as the loss of ΔΨm induced by OGD. Taken together, our results demonstrate for the first time that the AIF-mediated mitochondrial pathway plays a critical role in the protective effect of diazoxide against SH-SY5Y cell apoptosis induced by OGD. Diazoxide treatment might represent a novel therapeutic target for the treatment of ischemic cerebrovascular diseases.
journal_name
Brain Resjournal_title
Brain researchauthors
Zhang H,Wang ZQ,Zhao DY,Zheng DM,Feng J,Song LC,Luo Ydoi
10.1016/j.brainres.2010.11.019subject
Has Abstractpub_date
2011-01-25 00:00:00pages
89-98eissn
0006-8993issn
1872-6240pii
S0006-8993(10)02503-5journal_volume
1370pub_type
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