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坏死抑制因子-1对NRK-52E肾小管上皮细胞系细胞死亡的流量控制作用

Flow control effect of necrostatin-1 on cell death of the NRK-52E renal tubular epithelial cell line.

作者信息

Luo Jialun, Tao Yiming, Liang Xinling, Chen Yuanhan, Zhang Li, Jiang Fen, Liu Shuangxin, Ye Zhiming, Li Zhilian, Shi Wei

机构信息

Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.

Department of Nephrology, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong 510080, P.R. China.

出版信息

Mol Med Rep. 2017 Jul;16(1):57-62. doi: 10.3892/mmr.2017.6556. Epub 2017 May 9.

DOI:10.3892/mmr.2017.6556
PMID:28487950
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5482151/
Abstract

Apoptosis and necroptosis occur in renal tubular epithelial cell (RTEC) death in acute kidney injury (AKI), and may be regulated by several methods. The present study identified a protective effect of necrostatin‑1 (Nec‑1) on RTECs via a flow-control-like effect. The results established a hypoxic‑ischemic injury model of rat NRK‑52E RTECs using tumour necrosis factor‑α followed by ATP depletion with antimycin A and the pan-caspase pathway blocker, benzyloxycarbonyl-Val-Ala-Asp-fluoro-methylketone. Following pre‑treatment of cells with Nec‑1, cell organelle inflation, fragmentation inhibition and improved cell viability were observed with a parallel reduced expression of microtubule‑associated protein 1A/1B‑light chain 3‑II. Nec‑1 was involved in flow control in the process of cell injury and death. In conclusion, the present study indicated that Nec‑1 provides a protective effect and serves an important role in the prevention of AKI in an NRK‑52E cell model. Further studies will be required to fully investigate the role of Nec‑1 in the development of AKI in vivo.

摘要

凋亡和坏死性凋亡在急性肾损伤（AKI）时肾小管上皮细胞（RTEC）死亡过程中发生，且可能受多种方式调控。本研究通过类似流量控制的效应确定了坏死抑制因子-1（Nec-1）对RTEC的保护作用。研究结果利用肿瘤坏死因子-α建立大鼠NRK-52E RTEC的缺氧缺血损伤模型，随后用抗霉素A消耗ATP以及使用泛半胱天冬酶途径阻断剂苄氧羰基-Val-Ala-Asp-氟甲基酮。在用Nec-1预处理细胞后，观察到细胞器肿胀、碎片形成受到抑制且细胞活力提高，同时微管相关蛋白1A/1B轻链3-II的表达平行降低。Nec-1在细胞损伤和死亡过程中参与流量控制。总之，本研究表明Nec-1具有保护作用，在NRK-52E细胞模型中预防AKI方面发挥重要作用。需要进一步研究以全面探究Nec-1在体内AKI发生发展中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/99235b07a154/MMR-16-01-0057-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/8e388f2ec746/MMR-16-01-0057-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/21ad1795e0db/MMR-16-01-0057-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/6bb6f4ad3be5/MMR-16-01-0057-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/a2d8d1c965b1/MMR-16-01-0057-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/c41483607887/MMR-16-01-0057-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/99235b07a154/MMR-16-01-0057-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/8e388f2ec746/MMR-16-01-0057-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/21ad1795e0db/MMR-16-01-0057-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/6bb6f4ad3be5/MMR-16-01-0057-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/a2d8d1c965b1/MMR-16-01-0057-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/c41483607887/MMR-16-01-0057-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6312/5482151/99235b07a154/MMR-16-01-0057-g05.jpg

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