ArticleJournal of molecular neuroscience : MN2013
Role of paraoxonase-1 in the protection of hydrogen sulfide-donating sildenafil (ACS6) against homocysteine-induced neurotoxicity.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Hydrogen sulfide in precision medicine: connecting basic science, sensing, and clinical application.Medical gas research · 2026Review
- Transsulfuration Pathway Products and HInternational journal of molecular sciences · 2025Review
- Pills of Multi-Target HInternational journal of molecular sciences · 2024Review
- Research Progress of HMolecules (Basel, Switzerland) · 2022Review
- Hydrogen Sulfide (HCurrent neuropharmacology · 2022Review
- Hydrogen sulfide attenuates chronic restrain stress-induced cognitive impairment by upreglulation of Sirt1 in hippocampus.Oncotarget · 2017Article
- International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of HPharmacological reviews · 2017Review
- HCellular and molecular life sciences : CMLS · 2017Review
- Hydrogen sulfide: physiological properties and therapeutic potential in ischaemia.British journal of pharmacology · 2015Review
- Role of Hydrogen Sulfide in Ischemia-Reperfusion Injury.Oxidative medicine and cellular longevity · 2015Review
- Role of hydrogen sulfide in brain synaptic remodeling.Methods in enzymology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ACS6, a novel hydrogen sulfide (H2S)-releasing sildenafil, has been demonstrated to inhibit superoxide formation through donating H2S. We have previously found that ACS6 antagonizes homocysteine-induced apoptosis and cytotoxicity. The aim of the present study is to explore the molecular mechanisms underlying ACS6-exerted protective action against the neurotoxicity of homocysteine. In the present work, we used PC12 cells to explore whether paraoxonase-1 (PON-1) is implicated in ACS6-induced neuroprotection against homocysteine neurotoxicity. We show that ACS6 treatment results in prevention of homocysteine-caused neurotoxicity and overproduction of reactive oxygen species (ROS). Homocysteine downregulates the expression and activity of PON-1; however, this effect is significantly blocked by co-treatment with ACS6. The specific inhibitor of PON-1 2-hydroxyquinoline reverses the inhibitory effect of ACS6 on homocysteine-induced neurotoxicity and intracellular ROS accumulation. These results indicate that ACS6 protects PC12 cells against homocysteine-induced neurotoxicity by upregulating PON-1 and suggest a promising role of PON-1 as a novel therapeutic strategy for homocysteine-induced toxicity.
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Registered trials
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