ArticleBiomedical reports2017
NADPH oxidase inhibitor, diphenyleneiodonium prevents necroptosis in HK-2 cells.
Article in Biomedical reports, 2017. 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, 17 citations in OpenAlex.
- Decoding ferroptosis and apoptosis crosstalk in glioblastoma: molecular mechanisms, microenvironmental regulation, and therapeutic advances.Molecular biology reports · 2026Review
- Nano-PROTACs for precision medicine: engineering strategies for enhanced targeting and potency.Journal of nanobiotechnology · 2026Review
- NETosis as an oncologic therapeutic target: a mini review.Frontiers in immunology · 2023Review
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- Article
- Astaxanthin induces NADPH oxidase activation and receptor‑interacting protein kinase 1‑mediated necroptosis in gastric cancer AGS cells.Molecular medicine reports · 2021Article
- Incorporating Transcriptomic-Metabolomic analysis reveal the effect of ultrasound on ethanol production in Saccharomyces Cerevisiae.Ultrasonics sonochemistry · 2021Review
- Inhibition of phase-1 biotransformation and cytostatic effects of diphenyleneiodonium on hepatoblastoma cell line HepG2 and a CYP3A4-overexpressing HepG2 cell clone.Clinical hemorheology and microcirculation · 2021Article
- Inhibition of NADPH oxidase alleviates germ cell apoptosis and ER stress during testicular ischemia reperfusion injury.Saudi journal of biological sciences · 2020Article
- Guidelines for evaluating myocardial cell death.American journal of physiology. Heart and circulatory physiology · 2019Review
- The role of necroptosis in the treatment of diseases.BMB reports · 2018Review
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the protective effect of the NADPH oxidase inhibitor, diphenyleneiodonium (DPI) against necroptosis in renal tubular epithelial cells. A necroptosis model of HK-2 cells was established using tumor necrosis factor-α, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone and antimycin A (collectively termed TZA), as in our previous research. The necroptosis inhibitor, necrostatin-1 (Nec-1) or the NADPH oxidase inhibitor, DPI were administered to the necroptosis model. Production of reactive oxygen species (ROS) was detected by dichlorodihydrofluorescein diacetate in the different groups, and the manner of cell death was identified by flow cytometry. Western blot analysis was used to determine the levels of phosphorylation of receptor-interacting protein kinase 3 (RIP-3) and mixed lineage kinase domain-like (MLKL), which are essential to necroptosis. The results revealed that TZA increased the percentages of propidium iodide-positive HK-2 cells from 1.22±0.69 to 8.98±0.73% (P<0.001), and augmented the phosphorylation of RIP-3 and MLKL. ROS levels were increased in the TZA group compared with the control group (27.74±1.60×10
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