ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2019
Hydrogen sulfide protects H9c2 cardiomyoblasts against H2O2-induced apoptosis.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- In Vitro Study on the Effects ofInternational journal of molecular sciences · 2026Article
- Influence of pigment epithelium-derived factors on HBiological research · 2025Article
- Hydrogen sulfide and ferroptosis inhibition underlies the dietary restriction-induced protection against cyclophosphamide cystitis.Frontiers in pharmacology · 2025Article
- Cardioprotective effect of Robinin ameliorates Endoplasmic Reticulum Stress and Apoptosis in H9c2 cells.Cell biochemistry and biophysics · 2024Article
- Carbon monoxide as a cellular protective agent in a swine model of cardiac arrest protocol.PloS one · 2024Article
- Asterarcys quadricellulare (Chlorophyceae) protects H9c2 cardiomyoblasts from HMolecular and cellular biochemistry · 2023Article
- Emerging roles of cystathionine β-synthase in various forms of cancer.Redox biology · 2022Review
- Carbon monoxide and a change of heart.Redox biology · 2021Review
- The Potential of Hydrogen Sulfide Donors in Treating Cardiovascular Diseases.International journal of molecular sciences · 2021Review
- Two novel anticancer compounds with minimum cardiotoxic property.BMC pharmacology & toxicology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) are highly reactive chemical species that may cause irreversible tissue damage, and play a critical role in cardiovascular diseases. Hydrogen sulfide (H2S) is a gasotransmitter that acts as a ROS scavenger with cardio-protective effects. In this study, we investigated the cytoprotective effect of H2S against H2O2-induced apoptosis in cardiomyocytes. H9c2 rat cardiomyoblasts were treated with H2S (100 μM) 24 h before challenging with H2O2 (100 μM). Apoptosis was then assessed by annexin V and PI, and mitochondrial membrane potential was measured using a fluorescent probe, JC-1. Our results revealed that H2S improved cell viability, reduced the apoptotic rate, and preserved mitochondrial membrane potential. An increased Bcl-2 to Bax ratio was also seen in myocytes treated with H2S after H2O2-induced stress. Our findings indicated a therapeutic potential for H2S in preventing myocyte death following ischemia/reperfusion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.