Upregulated dual oxidase 1-induced oxidative stress and caspase-1-dependent pyroptosis reflect the etiologies of heart failure

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Yan Song Li, Jingwen Xia, Chang Yuan Chen, Shu Hong Ren, Mao Rong He
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Abstract

Oxidative stress is implicated in the pathogenesis of heart failure. Dual oxidase 1 (DUOX1) might be important in heart failure development through its mediating role in oxidative stress. This study was designed to evaluate the potential role of DUOX1 in heart failure. AC16 cells were treated with 2 µmol/L of doxorubicin (DOX) for 12, 24, and 48 h to construct a heart failure model. DUOX1 overexpression and silencing in AC16 cell were established. DUOX1 expression was detected by Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Pyroptosis and reactive oxygen species (ROS) production were measured by flow cytometry. Increased DUOX1 expression levels were observed after DOX treatment for 24 h in AC16 cells. DUOX1 silencing inhibited DOX-induced pyroptosis and ROS production. The release of IL-1β, IL-18, and lactate dehydrogenase (LDH), and expression levels of pyroptosis-related proteins were also decreased. DUOX1 overexpression increased pyroptosis, ROS production, IL-1β, IL-18, and LDH release, and pyroptosis-related protein expression. N-acetyl-cysteine (NAC) significantly reversed DUOX1-induced pyroptosis, ROS, and related factors. These results suggest that DUOX1-derived genotoxicity could promote heart failure development. In the process, oxidative stress and pyroptosis may be involved in the regulation of DUOX1 in heart failure.
双氧化酶 1 诱导的氧化应激上调和 caspase-1 依赖性热解反映了心力衰竭的病因
氧化应激与心力衰竭的发病机制有关。双重氧化酶 1(DUOX1)可能通过其在氧化应激中的介导作用而在心力衰竭的发病过程中发挥重要作用。本研究旨在评估 DUOX1 在心衰中的潜在作用。用 2 µmol/L 的多柔比星(DOX)处理 AC16 细胞 12、24 和 48 小时,以构建心衰模型。建立了 AC16 细胞中 DUOX1 的过表达和沉默。通过定量实时聚合酶链反应(qRT-PCR)和免疫印迹检测DUOX1的表达。流式细胞术检测了热休克和活性氧(ROS)的产生。AC16 细胞经 DOX 处理 24 小时后,观察到 DUOX1 表达水平升高。沉默DUOX1可抑制DOX诱导的热休克和ROS产生。IL-1β、IL-18和乳酸脱氢酶(LDH)的释放以及热解相关蛋白的表达水平也有所下降。DUOX1 的过表达增加了热变态反应、ROS 的产生、IL-1β、IL-18 和 LDH 的释放以及热变态反应相关蛋白的表达。N-乙酰半胱氨酸(NAC)能明显逆转 DUOX1 诱导的热休克、ROS 和相关因子。这些结果表明,DUOX1 衍生的基因毒性可促进心力衰竭的发生。在此过程中,氧化应激和热蛋白沉积可能参与了心衰中 DUOX1 的调控。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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