dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorUniversidad San Sebastián
dc.creatorBaez, Eliana
dc.creatorGuio-Vega, Gina Paola
dc.creatorEcheverria, Valentina
dc.creatorSandoval-Rueda, Daniel Andres
dc.creatorBarreto, George E.
dc.date.accessioned2023-05-24T04:28:10Z
dc.date.available2023-05-24T04:28:10Z
dc.date.created2023-05-24T04:28:10Z
dc.date.issued2017-08-01
dc.identifier1029-8428
dc.identifierhttps://repositorio.uss.cl/handle/uss/4361
dc.identifier10.1007/s12640-017-9733-x
dc.description.abstractThe translocator protein (TSPO), formerly known as the peripheral-type benzodiazepine receptor (PBR), is considered an important regulator of steroidogenesis and a potential therapeutic target in neurological disorders. Previous evidence suggests that TSPO ligands can protect cells during injury and prevent apoptosis in central nervous system (CNS) cells. However, its actions on astrocytic cells under metabolic injury are not well understood. In this study, we explored whether 4′-chlorodiazepam (Ro5–4864), a TSPO ligand, might protect astrocyte mitochondria under glucose deprivation. Our results showed that 4′-chlorodiazepam preserved cell viability and reduced nuclear fragmentation in glucose-deprived cells. These effects were accompanied by a reduced production of free radicals and maintenance of mitochondrial functions in cells treated with 4′-chlorodiazepam. Finally, our findings suggest that TSPO might be involved in reducing oxidative stress by preserving mitochondrial functions in astrocytic cells exposed to glucose withdrawal.
dc.languageeng
dc.relationNeurotoxicity Research
dc.title4′-Chlorodiazepam Protects Mitochondria in T98G Astrocyte Cell Line from Glucose Deprivation
dc.typeArtículo


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