RIP1 mediates the protection of geldanamycin on neuronal injury induced by oxygen-glucose deprivation combined with zVAD in primary cortical neurons.
作者： Wei-Wei Chen , Hailong Yu , Hong-Bin Fan , Cui-Cui Zhang , Min Zhang
DOI: 10.1111/J.1471-4159.2011.07526.X
关键词:
摘要: Caspase-dependent apoptosis is considered one of the most important cell death pathways. When apoptotic process blocked, a form programmed necrosis called necroptosis occurs. Apoptosis and may share some regulatory mechanisms. Recent studies indicated that receptor interacting protein 1 (RIP1), an Hsp90-associated kinase, switch between necroptosis. In this study, we showed oxygen-glucose deprivation (OGD) combined with caspase inhibitor zVAD (OGD/zVAD)-induced RIP1 expression in time-dependent manner. We found geldanamycin (GA), benzoquinone ansamycin, protected against neuronal injury induced by OGD/zVAD treatment cultured primary neurons. More importantly, GA decreased level time- concentration-dependent also Hsp90 level, which caused instability protein, resulting but not mRNA after treatment. concluded GA-mediated protection OGD/zVAD-induced was associated enhanced decreasing level. its derivatives be promising for prevention during ischemic injury.
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