NADPH oxidase inhibitor, diphenyleneiodonium prevents necroptosis in HK-2 cells
| Autor: | Ruizhao Li, Li Zhang, Bin Zhang, Shuangxin Liu, Wei Dong, Xinling Liang, Zhiming Ye, Wei Shi, Jialun Luo, Huaban Liang, Chunling Li, Zhilian Li, Yuanhan Chen, Lixia Xu, Weidong Wang |
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| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
chemistry.chemical_classification Reactive oxygen species Programmed cell death NADPH oxidase Necrosis biology General Neuroscience Necroptosis General Medicine Articles Molecular biology General Biochemistry Genetics and Molecular Biology Cell biology 03 medical and health sciences 030104 developmental biology chemistry Apoptosis biology.protein medicine Tumor necrosis factor alpha General Pharmacology Toxicology and Pharmaceutics medicine.symptom Protein kinase A |
| Popis: | 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 |
| Databáze: | OpenAIRE |
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