A New Hope for a Devastating Disease: Hydrogen Sulfide in Parkinson’s Disease

• Published in: Molecular neurobiology Vol. 55; no. 5; pp. 3789 - 3799
• Main Authors: Cao, Xu, Cao, Lei, Ding, Lei, Bian, Jin-song
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.05.2018; Springer Nature B.V
• Subjects: 6-Hydroxydopamine; Animals; Apoptosis; Apoptosis - physiology; Biomedical and Life Sciences; Biomedicine; Brain - metabolism; Calcium (intracellular); Calcium homeostasis; Carbon monoxide; Cell Biology; Disease Models, Animal; Glutamic acid receptors (ionotropic); Homeostasis; Humans; Hydrogen sulfide; Hydrogen Sulfide - metabolism; Movement disorders; N-Methyl-D-aspartic acid receptors; Neurobiology; Neurodegenerative diseases; Neurology; Neuronal-glial interactions; Neurons - metabolism; Neurosciences; Nitric oxide; Oxidation; Parkinson Disease - metabolism; Parkinson's disease; Substantia nigra; Supplements; Hydrogen sulfide; S donors; H; Protective effect; Brain modulation; Anti-oxidation; Parkinson’s disease; H2S donors
• ISSN: 0893-7648; 1559-1182
• DOI: 10.1007/s12035-017-0617-0

Hydrogen sulfide (H 2 S) has been regarded as the third gaseous transmitter alongside nitric oxide (NO) and carbon monoxide (CO). In mammalian brain, H 2 S is produced redundantly by four enzymatic pathways, implying its abundance in the organ. In physiological conditions, H 2 S has been found to induce the formation of long-term potential in neuronal cells by augmenting the activity of N-methyl-D-aspartate (NMDA) receptor. Likewise, it also actively takes part in the regulation of intracellular Ca 2+ and pH homeostasis in both neuronal cells and glia cells. Intriguingly, emerging evidence indicates a connection of H 2 S with Parkinson’s disease. Specifically, the endogenous H 2 S level in the substantia nigra (SN) is significantly reduced along with 6-hydroxydopamine (6-OHDA) treatment in rats, while supplementation of H 2 S not only reverses 6-OHDA-induced neuronal loss but also attenuates the following disorders of movement, suggesting a protective effect of H 2 S in Parkinson’s disease (PD). Remarkably, the protective effect has been extensively demonstrated with various in vitro and in vivo PD models. These suggest that H 2 S may be a new hope for the treatment of PD. Further studies have shown that the protective effects can be ascribed to H 2 S-mediated anti-oxidation, anti-inflammation, anti-apoptosis, and pro-survival activity, which are also summarized in the review. Moreover, the progresses on the development of H 2 S donors are also conveyed with an emphasis on the treatment of PD. Nevertheless, one should bear in mind that the precise role of H 2 S in the pathogenesis of PD remains largely elusive. Therefore, more studies are warranted before turning the hope into a real therapy for PD.