Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells

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

doi:10.3892/ijmm.2017.3227

Neuroprotective effects of hydrogen sulfide on sodium azide-induced oxidative stress in PC12 cells

Authors:
- Cheng Gao
- Pan Chang
- Lijun Yang
- Yi Wang
- Shaohua Zhu
- Haiyan Shan
- Mingyang Zhang
- Luyang Tao
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Affiliations: Key Laboratory of Evidence Science, China University of Political Science and Law, Ministry of Education, Beijing 100088, P.R. China, Central Laboratory, The Second Affiliated Hospital of Xi'an Medical College, Xi'an, Shaanxi 710038, P.R. China, Institute of Forensic Sciences, Soochow University, Suzhou, Jiangsu 215123, P.R. China, Department of Obstetrics and Gynecology, North District of Suzhou Municipal Hospital, Suzhou, Jiangsu 215000, P.R. China
Published online on: November 1, 2017 https://doi.org/10.3892/ijmm.2017.3227
Pages: 242-250
Copyright : © Gao et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

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Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder, responsible for >50% of all dementia cases. Sodium azide (NaN3) inhibits cytochrome oxidase by irreversibly binding to the heme cofactor and selectively reducing the complex IV activity, which is present in post‑mortem AD brains. Previous data demonstrated that hydrogen sulfide (H2S), the third endogenous gaseous mediator, exerted protective effects against neuronal damage. Therefore, it was hypothesized that H2S may be able to scavenge excess reactive oxygen species (ROS), thereby protecting against oxidative stress and cell death. In the present study, it was observed that cell viability decreased in a concentration-dependent manner 12 h after NaN3 treatment (20, 30 and 50 mmol/l). A decrease in cell viability (to 51±3%) was observed 12 h after treatment with 30 mM NaN3. NaN3 treatment also led to decreased mitochondrial membrane potential, increased lipid peroxidation (excessive production of malondialdehyde), and increased the protein expression levels of caspase-3. Pretreatment with H2S (200 µmol/l) attenuated NaN3-mediated apoptosis, and the anti-apoptotic action of H2S was partially dependent on suppressing the production of ROS. The findings of the present study suggested that H2S exerted a neuroprotective effect against NaN3-induced neurotoxicity through mechanisms related to anti-oxidation and anti-apoptosis. Therefore, the findings of the present study suggest there may be a promising future for H2S-based preventions and therapies for neuronal damage following exposure to NaN3.

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