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Hydrogen sulfide alleviates oxidative stress injury and reduces apoptosis induced by MPP+ in Parkinson’s disease cell model

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Abstract

Hydrogen sulfide (H2S), an endogenously produced gas, is a cardioprotective agent against neurotoxin-induced neurodegeneration in Parkinson's disease (PD). However, the roles of H2S in 1-methyl-4-phenylpyridinium ion (MPP+)-treated SH-SY5Y cells with the involvement of reactive oxygen species-nitric oxide (ROS-NO) signaling pathway in PD remain unclear. For this study, a MPP+-treated SH-SY5Y cell model was established to explore the regulatory role of H2S in oxidative stress injury and cell apoptosis. With the cell viability, apoptosis, cytotoxicity, levels of reactive oxygen species (ROS) and nitric oxide (NO), mitochondrial transmembrane potential (Δψm), contents of oxidative stress injury-related markers (glutathione, superoxide dismutase, malondialdehyde), levels of apoptosis-related proteins (Caspase 3, Bax, Bcl-2) and inducible nitric oxide synthase (iNOS) determined, this study demonstrated that NaHS (an H2S donor) treatment could alleviated the reduction of cell viability and cytotoxicity, cell apoptosis, Δψm loss, contents of ROS and NO, and oxidative stress injury induced by MPP+. The present study showed that H2S may protect SH-SY5Y cells from MPP+-induced injury in PD cell model via the inhibition of ROS-NO signaling pathway and provide insight into the potential of H2S for PD therapy.

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LL is the guarantor of integrity of the entire study and the study concepts; JW and HW contributed to the experimental studies, data acquisition and data analysis; LL contributed to the manuscript preparation; JW contributed to the manuscript editing. All authors read and approved the final manuscript. All authors have read the manuscript and authorized the submission for publication.

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Correspondence to Heng Wang.

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Liu, L., Wang, J. & Wang, H. Hydrogen sulfide alleviates oxidative stress injury and reduces apoptosis induced by MPP+ in Parkinson’s disease cell model. Mol Cell Biochem 472, 231–240 (2020). https://doi.org/10.1007/s11010-020-03801-y

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  • DOI: https://doi.org/10.1007/s11010-020-03801-y

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