Neuroprotective effects of hydrogen sulfide on sodium azide‑induced autophagic cell death in PC12 cells

Shan,Haiyan; Chu,Yang; Chang,Pan; Yang,Lijun; Wang,Yi; Zhu,Shaohua; Zhang,Mingyang; Tao,Luyang

doi:10.3892/mmr.2017.7363

Neuroprotective effects of hydrogen sulfide on sodium azide‑induced autophagic cell death in PC12 cells

Authors:
- Haiyan Shan
- Yang Chu
- Pan Chang
- Lijun Yang
- Yi Wang
- Shaohua Zhu
- Mingyang Zhang
- Luyang Tao
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Affiliations: Shanghai Key Laboratory of Forensic Medicine, Institute of Forensic Science, Ministry of Justice, Shanghai 200063, P.R. China, Institute of Forensic Sciences, Soochow University, Suzhou, Jiangsu 215123, P.R. China, Central Laboratory, Second Affiliated Hospital of Xi'an Medical College, Xi'an, Shaanxi 710038, P.R. China
Published online on: August 25, 2017 https://doi.org/10.3892/mmr.2017.7363
Pages: 5938-5946
Copyright: © Shan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Sodium azide (NaN3) is a chemical of rapidly growing commercial importance. It is very acutely toxic and inhibits cytochrome oxidase (COX) by binding irreversibly to the heme cofactor. A previous study from our group demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator identified, had protective effects against neuronal damage induced by traumatic brain injury (TBI). It is well‑known that TBI can reduce the activity of COX and have detrimental effects on the central nervous system metabolism. Therefore, in the present study, it was hypothesized that H2S may provide neuroprotection against NaN3 toxicity. The current results revealed that NaN3 treatment induced non‑apoptotic cell death, namely autophagic cell death, in PC12 cells. Expression of the endogenous H2S‑producing enzymes, cystathionine‑β‑synthase and 3‑mercaptopyruvate sulfurtransferase, decreased in a dose‑dependent manner following NaN3 treatment. Pretreatment with H2S markedly attenuated the NaN3‑induced cell viability loss and autophagic cell death in a dose‑dependent manner. The present study suggests that H2S‑based strategies may have future potential in the prevention and/or therapy of neuronal damage following NaN3 exposure.

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