亲爱的研友该休息了!由于当前在线用户较少,发布求助请尽量完整地填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!身体可是革命的本钱,早点休息,好梦!

Silica nanoparticles induce cardiac injury and dysfunction via ROS/Ca2+/CaMKII signaling

化学 活性氧 氧化应激 细胞凋亡 内科学 背景(考古学) 纤维化 细胞内 内分泌学 线粒体 细胞生物学 医学 生物 生物化学 古生物学
作者
Yi Qi,Hailin Xu,Xueyan Li,Xinying Zhao,Yan Li,Xianqing Zhou,Siyu Chen,Ning Shen,Rui Chen,Yanbo Li,Zhiwei Sun,Caixia Guo,Zhiwei Sun,Caixia Guo
出处
期刊:Science of The Total Environment [Elsevier BV]
卷期号:837: 155733-155733 被引量:39
标识
DOI:10.1016/j.scitotenv.2022.155733
摘要

Interest is growing to better comprehend the interaction of silica nanoparticles (SiNPs) with the cardiovascular system. In particular, the extremely small size, relatively large surface area and associated unique properties may greatly enhance its toxic potentials compared to larger-sized counterparts. Nevertheless, the underlying mechanisms still need to be evaluated. In this context, the cardiotoxicity of nano-scale (Si-60; particle diameter about 60 nm) and submicro-scale silica particles (Si-300; 300 nm) were examined in ApoE-/- mice via intratracheal instillation, 6.0 mg/kg·bw, once per week for 12 times. The echocardiography showed that the sub-chronic exposure of Si-60 declined cardiac output (CO) and stroke volume (SV), shorten LVIDd and LVIDs, and thickened LVAWs of ApoE-/- mice in compared to the control and Si-300 groups. Histological investigations manifested Si-60 enhanced inflammatory infiltration, myocardial fiber arrangement disorder, hypertrophy and fibrosis in the cardiac tissue, as well as mitochondrial ultrastructural injury. Accordingly, the serum cTnT, cTnI and ANP were significantly elevated by Si-60, as well as cardiac ANP content. In particular, Si-60 greatly increased cardiac ROS, Ca2+ levels and CaMKII activation in comparison with Si-300. Further, in vitro investigations revealed silica particles induced a dose- and size-dependent activation of oxidative stress, mitochondrial membrane permeabilization, intracellular Ca2+ overload, CaMKII signaling activation and ensuing myocardial apoptosis in human cardiomyocytes (AC16). Mechanistic analyses revealed SiNPs induced myocardial apoptosis via ROS/Ca2+/CaMKII signaling, which may contribute to the abnormalities in cardiac structure and function in vivo. In summary, our research revealed SiNPs caused myocardial impairments, dysfunction and even structural remodeling via ROS/Ca2+/CaMKII signaling. Of note, a size-dependent myocardial toxicity was noticed, that is, Si-60 greater than Si-300.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
hlt完成签到 ,获得积分10
2秒前
高大的羿发布了新的文献求助10
2秒前
南吕十八发布了新的文献求助10
2秒前
5秒前
7秒前
RCJ发布了新的文献求助10
10秒前
NaiVe发布了新的文献求助10
14秒前
18秒前
22秒前
yaya发布了新的文献求助10
25秒前
喜悦宫苴完成签到,获得积分10
27秒前
放开让我学习完成签到,获得积分10
28秒前
科研通AI6.4应助hh采纳,获得30
28秒前
2058753794完成签到 ,获得积分10
29秒前
29秒前
风中的断缘完成签到,获得积分10
30秒前
忧郁小丑完成签到 ,获得积分10
31秒前
科研通AI6.3应助xny采纳,获得10
31秒前
yaya完成签到,获得积分10
31秒前
32秒前
32秒前
合一海盗完成签到,获得积分10
32秒前
ada阿达完成签到,获得积分10
32秒前
嘻嘻哈哈应助科研通管家采纳,获得10
32秒前
33秒前
33秒前
33秒前
JamesPei应助科研通管家采纳,获得10
33秒前
慕青应助科研通管家采纳,获得10
33秒前
汉堡包应助含蓄薯片采纳,获得10
36秒前
36秒前
茶柠完成签到 ,获得积分10
38秒前
烽火戏诸侯完成签到,获得积分20
41秒前
Seven完成签到 ,获得积分10
42秒前
43秒前
十三完成签到,获得积分10
47秒前
Leofar完成签到 ,获得积分10
47秒前
xzy998应助烽火戏诸侯采纳,获得10
48秒前
明月朗晴完成签到 ,获得积分10
49秒前
51秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Inorganic Chemistry Eighth Edition 1200
Free parameter models in liquid scintillation counting 1000
Anionic polymerization of acenaphthylene: identification of impurity species formed as by-products 1000
Standards for Molecular Testing for Red Cell, Platelet, and Neutrophil Antigens, 7th edition 1000
The Organic Chemistry of Biological Pathways Second Edition 800
The Psychological Quest for Meaning 800
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6313242
求助须知:如何正确求助?哪些是违规求助? 8129760
关于积分的说明 17036644
捐赠科研通 5369914
什么是DOI,文献DOI怎么找? 2851118
邀请新用户注册赠送积分活动 1828916
关于科研通互助平台的介绍 1681048