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Iranian Journal of Basic Medical Sciences، جلد ۲۱، شماره ۸، صفحات ۸۶۳-۸۶۸
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عنوان انگلیسی Hypoxia-reoxygenation induced necroptosis in cultured rat renal tubular epithelial cell line
چکیده انگلیسی مقاله Objective(s): The aim of this study is to explore the potential role of hypoxia/reoxygenation in necroptosis in cultured rat renal tubular epithelial cell line NRK-52E, and further to investigate its possible mechanisms.Materials and Methods: Cells were cultured under different hypoxia-reoxygenation conditions                        in vitro. MTT assay was used to measure the cell proliferation of cells that were exposed to hypoxia-reoxygenation conditions at different time points. Receptor-interacting protein 1,3 (RIP1 and RIP3) and NF-κB were detected by Western-blot analysis. Co-immunoprecipitation (Co-IP) was conducted to investigate the formation of necrosome. Necrostatin-1 (Nec-1) was adopted to inhibit the occurrence of necroptosis. In addition, morphological changes of cells after hypoxia-reoxygenation interference were observed under transmission electron microscope (TEM).  Results: MTT assay indicated that hypoxia-reoxygenation treatment can cause a decrease in cell viability. Particularly, 6 hr of hypoxia and 24 hr of reoxygenation (H6R24 group) resulted in the lowest cell viability. Western-blot results indicated that the expression of RIP3 significantly increased in H6R24 group while the expression of NF-κB is decreased. Co-IP results demonstrated that the interaction between RIP1 and RIP3 was stronger in the hypoxia-reoxygenation induced group than the other groups, furthermore, treatment with Nec-1 reduced the formation of necrosome. TEM observation results showed that hypoxia-reoxygenation treated cells showed typical morphological characteristics of necroptosis and autophagy.Conclusion: Hypoxia-reoxygenation treatment can induce necroptosis in NRK-52E cells, and this effect can be inhibited by Nec-1. In addition, the mechanism of necroptosis induced by hypoxia-reoxygenation injury on cells may be related to the low expression of NF-κB.
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نویسندگان مقاله | Changlai Zhu
Jiangsu Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, P. R. China


| Yang Liu
Jiangsu Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, P. R. China


| Zongyu Guan
Medical College of Nantong University, Nantong, JS, P. R. China


| Yi Zhou
Medical College of Nantong University, Nantong, JS, P. R. China


| Fang Liu
Jiangsu Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, P. R. China


| Tianyi Zhang
Jiangsu Key Laboratory of Neuroregeneration, Co-innovation Center of Neuroregeneration, Nantong University, Nantong, JS 226001, P. R. China
نشانی اینترنتی http://ijbms.mums.ac.ir/article_11091.html
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