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01.06.2015 | Research Article

Induction of DJ-1 protects neuronal cells from isoflurane induced neurotoxicity

Erschienen in: Metabolic Brain Disease | Ausgabe 3/2015

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Abstract

Oxidative stress, mitochondrial dysfunction and neuronal apoptosis are thought to be major contributors of Isoflurane toxicity. However, the underlying mechanisms remain largely to be determined. DJ-1, a protein that is involved in the response to various kinds of stress, has shown its neuroprotective effects. Whether DJ-1 has a neuroprotective effect against isoflurane-induced neurotoxocity is still unknown. In this study, we found that expression of DJ-1 is elevated in response to isoflurane treatment in human SH-SY5Y neuroblastoma cells. In order to clarify whether DJ-1 plays a potential role in isoflurane neurotoxicity or as a compensatory response for survival, we investigated the effects of DJ-1 silencing in isoflurane neurotoxicity. Our findings indicate that knockdown of DJ-1 promotes isoflurane-induced oxidative stress and mitochondrial dysfunction. Importantly, DJ-1 silencing was found to exacerbate isoflurane- induced apoptosis through modulation of mitochondria-dependent apoptosis pathways, thereby suggesting that induction of DJ-1 in response to isoflurane might act as a compensatory response for cell survival.

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Titel: Induction of DJ-1 protects neuronal cells from isoflurane induced neurotoxicity
Publikationsdatum: 01.06.2015
Erschienen in: Metabolic Brain Disease / Ausgabe 3/2015
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI: https://doi.org/10.1007/s11011-014-9622-4

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