Silver nanoparticles (AgNPs) have become increasingly popular in the biomedical field over the last few decades due to its proven antibacterial property. Previous scientific studies have reported that one of the major organs responsible for detoxification of AgNPs is the liver. The liver is also the primary organ responsible for secretion of angiotensinogen (AGT), a key signaling molecule involved in the renin-angiotensin system (RAS), which plays an important role in maintaining cardiac output and vascular pressure. The aim of this study was to assess any potential changes in the RAS-associated gene signaling, inflammatory response, and hepatocellular toxicity resulting from AgNP exposure. To do this, 6-week-old, male Wistar rats were exposed to a subacute inhalation exposure of AgNP (200 ppb/days over 4 h/days exposure, for 5 d) and their livers were analyzed for alterations in RAS components, inflammation, and oxidative stress. Real time qPCR analysis showed that AgNP-exposure resulted in a significant increase in hepatic AGT, angiotensin converting enzyme (ACE)-1, and ACE-2 mRNA expression. Expression of inflammatory markers interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α were also upregulated with AgNP-exposure, compared to controls. Furthermore AgNP-exposure mediated a significant increase in hepatic expression of catalase, and superoxide dismutase, and oxidative stress, as assessed via 8-Oxo-2′-deoxyguanosine staining. Increased oxidative stress was associated with increased monocyte/macrophage-2 staining in the liver of AgNP-exposed rats. Such findings indicate that subacute inhalation exposure to AgNPs mediate increased hepatic RAS signaling, associated with inflammation, macrophage infiltration, and oxidative stress.

中文翻译：

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在 Wistar 大鼠中，吸入银纳米粒子会诱发肝脏炎症和氧化应激，这与肾素-血管紧张素系统信号传导的改变有关

在过去的几十年中，银纳米粒子 (AgNPs) 由于其经过验证的抗菌特性而在生物医学领域变得越来越流行。先前的科学研究报告说，负责 AgNPs 解毒的主要器官之一是肝脏。肝脏也是负责分泌血管紧张素原 (AGT) 的主要器官，血管紧张素原是参与肾素-血管紧张素系统 (RAS) 的关键信号分子，在维持心输出量和血管压力方面发挥着重要作用。本研究的目的是评估 AgNP 暴露导致的 RAS 相关基因信号、炎症反应和肝细胞毒性的任何潜在变化。为此，将 6 周大的雄性 Wistar 大鼠暴露于 AgNP 亚急性吸入暴露（200 ppb/天超过 4 小时/天暴露，5 d) 并分析他们的肝脏中 RAS 成分、炎症和氧化应激的变化。实时 qPCR 分析表明，AgNP 暴露导致肝脏 AGT、血管紧张素转换酶 (ACE)-1 和 ACE-2 mRNA 表达显着增加。与对照组相比，AgNP 暴露也上调了炎症标志物白细胞介素 (IL)-6、IL-1β 和肿瘤坏死因子 (TNF)-α 的表达。此外，通过 8-Oxo-2'-脱氧鸟苷染色评估，AgNP 暴露介导过氧化氢酶、超氧化物歧化酶和氧化应激的肝脏表达显着增加。氧化应激增加与 AgNP 暴露大鼠肝脏中单核细胞/巨噬细胞 2 染色增加有关。这些发现表明，亚急性吸入暴露于 AgNPs 会介导肝脏 RAS 信号传导增加，