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dc.contributor.authorMohammad Alizadeh, E
dc.contributor.authorMahdavi, M
dc.contributor.authorJenani Fard, F
dc.contributor.authorChamani, S
dc.contributor.authorFarajdokht, F
dc.contributor.authorKarimi, P
dc.date.accessioned2018-08-26T04:52:55Z
dc.date.available2018-08-26T04:52:55Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/37740
dc.description.abstractOxidative stress has a causative role in ischemic reperfusion-induced cell death. Evidence has shown that metformin is capable to reduce ischemic reperfusion injuries. The current study investigated the effect of metformin on ischemia/reperfusion-induced apoptosis in PC12 cells by evaluation of Bcl-2 family proteins expression. Cells were exposed to a time-dependent in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) injury and then treated with metformin. The intracellular reactive oxygen species (ROS) levels were measured. Western blotting was used to examine the expression of anti- and pro-apoptotic proteins. Moreover, the number of apoptotic cell death was evaluated by TUNEL assay. Our results showed that metformin attenuated ROS generation, downregulated pro-apoptotic BAX expression, and upregulated expression of the Bcl-2 protein in the PC12 cells. Moreover, metformin reduced cell death under OGD/R condition which was confirmed by lower apoptotic cell death in the TUNEL assay. These findings suggest that neuroprotective effect of metformin on OGD/R-induced cell death is possibly mediated by inhibition of ROS-induced apoptosis pathway.
dc.language.isoEnglish
dc.relation.ispartofToxicology mechanisms and methods
dc.titleMetformin protects PC12 cells against oxygen-glucose deprivation/reperfusion injury.
dc.typearticle
dc.citation.spage1
dc.citation.epage8
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1080/15376516.2018.1486495


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