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Published on: May 12, 2018
Induction of DJ-1 protects neuronal cells from isoflurane induced neurotoxicity
Wenjie Liu1, Qulian Guo, Xiaoling Hu
1Department of Anesthesiology, Xiangya Hospital, Central South University, 87 Xiangya Road, 410008, Changsha, Hunan, China.
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.
Insights
DJ-1 protein protects against isoflurane toxicity by reducing oxidative stress and apoptosis. Silencing DJ-1 worsened isoflurane-induced neurotoxicity, suggesting DJ-1
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Isoflurane anesthesia can cause neurotoxicity.
- Oxidative stress, mitochondrial dysfunction, and apoptosis are key factors in this toxicity.
- DJ-1 protein is known for its stress-response and neuroprotective roles.
Purpose of the Study:
- To investigate the role of DJ-1 in isoflurane-induced neurotoxicity.
- To determine if DJ-1 acts as a protective mechanism against isoflurane's harmful effects.
Main Methods:
- Studied DJ-1 expression in human SH-SY5Y neuroblastoma cells treated with isoflurane.
- Utilized DJ-1 gene silencing (knockdown) to assess its impact on isoflurane toxicity.
- Analyzed oxidative stress, mitochondrial function, and apoptosis pathways.
Main Results:
- Isoflurane treatment increased DJ-1 expression in neuroblastoma cells.
- DJ-1 knockdown exacerbated isoflurane-induced oxidative stress and mitochondrial dysfunction.
- Silencing DJ-1 worsened isoflurane-induced apoptosis via mitochondria-dependent pathways.
Conclusions:
- Increased DJ-1 expression is a compensatory response to isoflurane exposure.
- DJ-1 plays a significant neuroprotective role against isoflurane toxicity.
- Targeting DJ-1 may offer therapeutic strategies for mitigating isoflurane-induced neurotoxicity.
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