Inhalation exposure to silver nanoparticles induces hepatic inflammation and oxidative stress, associated with altered renin-angiotensin system signaling, in Wistar rats.
Inhalation exposure to silver nanoparticles induces hepatic inflammation and oxidative stress, associated with altered renin-angiotensin system signaling, in Wistar rats.
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DOI：
10.1002/tox.23412
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发表时间：
2022-03
影响因子：
4.5
通讯作者：
Verbeck GF
中科院分区：
文献类型：
--
作者：
Nayek S;Lund AK;Verbeck GF
银纳米颗粒（AgNPs）由于其已被证实的抗菌特性在过去几十年中在生物医学领域中变得越来越受欢迎。以前的科学研究已经报道，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，其在维持心输出量和血管压力中起重要作用。本研究的目的是评估由AgNP暴露引起的RAS相关基因信号传导、炎症反应和肝细胞毒性的任何潜在变化。为此，将6周龄雄性Wistar大鼠暴露于亚急性AgNP吸入暴露（200 ppb/d，暴露4小时/d，持续5 d），并分析其肝脏RAS组分、炎症和氧化应激的变化。真实的时间qPCR分析显示，AgNP暴露导致肝脏AGT、血管紧张素转换酶（ACE）-1和ACE-2 mRNA表达显著增加。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-1 β和肿瘤坏死因子（TNF）-α的表达。此外，通过8-氧代-2'-脱氧鸟苷（8-OHdG）染色评估，AgNP暴露介导了过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的肝脏表达和氧化应激的显著增加。氧化应激增加与单核细胞/巨噬细胞（MOMA）-2染色在AgNP暴露大鼠的肝脏。这些发现表明亚急性吸入暴露于AgNP介导增加的肝脏RAS信号传导，与炎症、巨噬细胞浸润和氧化应激相关。
Silver nanoparticles (AgNPs) have become increasingly popular in the biomedical field over the last few decades due to its proven anti-bacterial 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 sub-acute inhalation exposure of AgNP (200 ppb/d over 4 hr/d exposure, for 5 d) and their livers were analysed 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 (CAT), and superoxide dismutase (SOD), and oxidative stress, as assessed via 8-Oxo-2’-deoxyguanosine (8-OHdG) staining. Increased oxidative stress was associated with increased monocyte/macrophage (MOMA)-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.
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DOI：
10.3390/nano6100189
发表时间：
2016-10-20
期刊：
Nanomaterials (Basel, Switzerland)
影响因子：
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