ArticleBritish journal of pharmacology2010
Protective effect of hydrogen sulphide against 6-OHDA-induced cell injury in SH-SY5Y cells involves PKC/PI3K/Akt pathway.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 103 citations in OpenAlex.
- Potential therapeutic applications of medical gases in cancer treatment.Medical gas research · 2025Review
- Investigating the antiproliferative mechanisms of NaHS, a hydrogen sulfide donor, in the SH-SY5Y cell line.Medical oncology (Northwood, London, England) · 2025Article
- Role of Hydrogen Sulfide in Oncological and Non-Oncological Disorders and Its Regulation by Non-Coding RNAs: A Comprehensive Review.Non-coding RNA · 2024Review
- The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023Review
- Targeting Homocysteine and Hydrogen Sulfide Balance as Future Therapeutics in Cancer Treatment.Antioxidants (Basel, Switzerland) · 2023Review
- Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022Review
- Hydrogen Sulfide (HCurrent neuropharmacology · 2022Review
- Hydrogen Sulfide Attenuates the Cognitive Dysfunction in Parkinson's Disease Rats via Promoting Hippocampal Microglia M2 Polarization by Enhancement of Hippocampal Warburg Effect.Oxidative medicine and cellular longevity · 2022Article
- Neuroprotective activity of natural products isolated from Senecio graciliflorus DC against corticosterone-induced impairment in SH-SY5Y cells.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Hydrogen Sulfide Actions in the Vasculature.Comprehensive Physiology · 2021Article
- The Hidden Role of Hydrogen Sulfide Metabolism in Cancer.International journal of molecular sciences · 2021Review
- Anti-aging Klotho Protects SH-SY5Y Cells Against Amyloid β1-42 Neurotoxicity: Involvement of Wnt1/pCREB/Nrf2/HO-1 Signaling.Journal of molecular neuroscience : MN · 2021Article
- Regulation of Actg1 and Gsta2 is possible mechanism by which capsaicin alleviates apoptosis in cell model of 6-OHDA-induced Parkinson's disease.Bioscience reports · 2020Article
- Neuroprotection of SAK3 on scopolamine-induced cholinergic dysfunction in human neuroblastoma SH-SY5Y cells.Cytotechnology · 2020Article
- Hydrogen Sulfide Protects Against Ammonia-Induced Neurotoxicity Through Activation of Nrf2/ARE Signaling in Astrocytic Model of Hepatic Encephalopathy.Frontiers in cellular neuroscience · 2020Article
- Hydrogen Sulfide Metabolism and Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- Norcepharadione B attenuates HExperimental biology and medicine (Maywood, N.J.) · 2019Article
- A Review of Hydrogen Sulfide Synthesis, Metabolism, and Measurement: Is Modulation of Hydrogen Sulfide a Novel Therapeutic for Cancer?Antioxidants & redox signaling · 2019Article
- Redox Mechanisms in Neurodegeneration: From Disease Outcomes to Therapeutic Opportunities.Antioxidants & redox signaling · 2019Review
- Cysteine Metabolism in Neuronal Redox Homeostasis.Trends in pharmacological sciences · 2018Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeHydrogen sulphide (H(2)S) is a novel neuromodulator. The present study aimed to investigate the protective effect of H(2)S against cell injury induced by 6-hydroxydopamine (6-OHDA), a selective dopaminergic neurotoxin often used to establish a model of Parkinson's disease for studying the underlying mechanisms of this condition. EXPERIMENTAL APPROACH: Cell viability in SH-SY5Y cells was measured using MTT assay. Western blot analysis and pharmacological manipulation were employed to study the signalling mechanisms. KEY
resultsTreatment of SH-SY5Y cells with 6-OHDA (50-200 microM) for 12 h decreased cell viability. Exogenous application of NaHS (an H(2)S donor, 100-1000 microM) or overexpression of cystathionine beta-synthase (a predominant enzyme to produce endogenous H(2)S in SH-SY5Y cells) protected cells against 6-OHDA-induced cell apoptosis and death. Furthermore, NaHS reversed 6-OHDA-induced loss of tyrosine hydroxylase. Western blot analysis showed that NaHS reversed the down-regulation of PKCalpha, epsilon and Akt and the up-regulation of PKCdelta in 6-OHDA-treated cells. Blockade of PKCalpha with Gö6976 (2 microM), PKCepsilon with EAVSLKPT (200 microM) or PI3K with LY294002 (20 microM) reduced the protective effects of H(2)S. However, inhibition of PKCdelta with rottlerin (5 microM) failed to affect 6-OHDA-induced cell injury. These data suggest that the protective effects of NaHS mainly resulted from activation of PKCalpha, epsilon and PI3K/Akt pathway. In addition, NaHS-induced Akt phosphorylation was significantly attenuated by Gö6976 and EAVSLKPT, suggesting that the activation of Akt by NaHS is PKCalpha, epsilon-dependent. CONCLUSIONS AND IMPLICATIONS: H(2)S protects SH-SY5Y cells against 6-OHDA-induced cell injury by activating the PKCalpha, epsilon/PI3K/Akt pathway.
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