ArticleInternational journal of molecular sciences2013
Protective effects of hydrogen sulfide in hypoxic human umbilical vein endothelial cells: a possible mitochondria-dependent pathway.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 44 citations in OpenAlex.
- TGF-β1 induces ROS to activate ferroptosis via the ERK1/2-WISP1 pathway to promote the progression of renal tubular epithelial cell fibrosis.Cytotechnology · 2025Article
- Emerging roles of hydrogen sulfide-metabolizing enzymes in cancer.Redox report : communications in free radical research · 2024Review
- Pan-inhibition of the three HCancer cell international · 2024Article
- Hydrogen sulfide against preeclampsia exposure-induced oxidative mitochondrial damage in HTR-8/SVneo cells.Frontiers in cardiovascular medicine · 2022Article
- LACTB induced apoptosis of oxaliplatin-resistant gastric cancer through regulating autophagy-mediated mitochondrial apoptosis pathway.American journal of translational research · 2021Article
- Macrophage migration inhibitory factor inhibition as a novel therapeutic approach against triple-negative breast cancer.Cell death & disease · 2020Article
- Dexmedetomidine alleviated neuropathic pain in dorsal root ganglion neurons by inhibition of anaerobic glycolysis activity and enhancement of ROS tolerance.Bioscience reports · 2020Article
- Smokeless tobacco extract inhibits proliferation and promotes apoptosis in oral mucous fibroblasts.Oncology letters · 2018Article
- The Increased Endogenous Sulfur Dioxide Acts as a Compensatory Mechanism for the Downregulated Endogenous Hydrogen Sulfide Pathway in the Endothelial Cell Inflammation.Frontiers in immunology · 2018Article
- Hydrogen Sulfide Protects against Chemical Hypoxia-Induced Injury via Attenuation of ROS-Mediated CaBioMed research international · 2018Article
- Hypoxia and hydrogen sulfide differentially affect normal and tumor-derived vascular endothelium.Redox biology · 2017Article
- The molecular mechanism of the anticancer effect of Artonin E in MDA-MB 231 triple negative breast cancer cells.PloS one · 2017Article
- TET2 Protects against oxLDL-Induced HUVEC Dysfunction by Upregulating the CSE/HFrontiers in pharmacology · 2017Article
- Hydrogen Sulfide Inhibits High Glucose-Induced sFlt-1 Production via Decreasing ADAM17 Expression in 3T3-L1 Adipocytes.International journal of endocrinology · 2017Article
- SIRT3 Mediates the Antioxidant Effect of Hydrogen Sulfide in Endothelial Cells.Antioxidants & redox signaling · 2016Article
- Iron stimulates plasma-activated medium-induced A549 cell injury.Scientific reports · 2016Article
- Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt.Oxidative medicine and cellular longevity · 2015Article
- Asymmetric synthesis and evaluation of danshensu-cysteine conjugates as novel potential anti-apoptotic drug candidates.International journal of molecular sciences · 2014Article
- Sodium hydrosulfide prevents myocardial dysfunction through modulation of extracellular matrix accumulation and vascular density.International journal of molecular sciences · 2014Article
- A H2S-Nampt dependent energetic circuit is critical to survival and cytoprotection from damage in cancer cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the study was to investigate the protective effects of sodium hydrosulfide (NaHS), a H2S donor, against hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs) and also to look into the possible mechanisms by which H2S exerts this protective effect. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and scratch wound healing assay were chosen to measure the cell viability and migration-promoting effects. The fluorescent probe, DCFH-DA and 5,5',6,6'-Tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide (JC-1) were applied to detect the reactive oxygen species (ROS) level and mitochondrial membrane potential (ΔΨm). Furthermore, western blots were used to measure the expressions of the apoptosis-related proteins. Under hypoxic conditions, 300 μM and 600 μM of H2S could protect HUVECs against hypoxia-induced injury, as determined by MTT assay. Following the treatment of 60 µM NaHS for 18 h, scratch wound healing assays indicated that the scratch became much narrower than control group. After treatment with 60 µM, 120 µM, and 600 µM NaHS, and hypoxia for 30 min, flow cytometry demonstrated that the ROS concentrations decreased to 95.08% ± 5.52%, 73.14% ± 3.36%, and 73.51% ± 3.05%, respectively, compared with the control group. In addition, the JC-1 assay showed NaHS had a protective effect on mitochondria damage. Additionally, NaHS increased Bcl-2 expression and decreased the expression of Bax, Caspase-3 and Caspase-9 in a dose-dependent way. Our results suggest that H2S can protect endothelial cells and promote migration under hypoxic condition in HUVECs. These effects are partially associated with the preservation of mitochondrial function mediated by regulating the mitochondrial-dependent apoptotic pathway.
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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 OpenQuestion graph.