褪黑素通过氧化应激和焦亡对黑磷纳米片肝毒性的保护作用。

IF 4.3 3区 化学 Q2 CHEMISTRY, MULTIDISCIPLINARY
ACS Omega Pub Date : 2024-11-11 eCollection Date: 2024-11-26 DOI:10.1021/acsomega.4c05889
Bo Zhang, Yuechen Xing, Youtong Guo, Shuo Jin, Xinran Shao, Jiaqi Fan, Chunyi Zhang, Yue Wang
{"title":"褪黑素通过氧化应激和焦亡对黑磷纳米片肝毒性的保护作用。","authors":"Bo Zhang, Yuechen Xing, Youtong Guo, Shuo Jin, Xinran Shao, Jiaqi Fan, Chunyi Zhang, Yue Wang","doi":"10.1021/acsomega.4c05889","DOIUrl":null,"url":null,"abstract":"<p><p>In the field of contemporary medicine, with the rapid application of nanomaterials, evaluating their biocompatibility and potential toxicity has become increasingly important. This study characterized black phosphorus nanosheets (BPNSs) and employed both in vivo and in vitro models to assess the impact of BPNSs exposure on oxidative stress and pyroptosis in hepatocytes. We investigated the hepatotoxicity of this emerging nanomaterial and the protective role of melatonin against BPNSs induced hepatocyte pyroptosis. The results showed that BPNSs exposure reduced hepatocyte viability, induced morphological changes, and elevated the expression of pyroptosis-related proteins, suggesting that BPNSs promote hepatocyte pyroptosis through the ROS-NLRP3-GSDMD pathway, thereby exacerbating the inflammatory response. Melatonin, a bioactive substance with anti-inflammatory and antioxidant properties, was found in our study to significantly mitigate these adverse effects. It emphasized the role of melatonin in regulating ROS production and related pathways, effectively protecting hepatocytes from BPNSs induced damage. This study elucidates the mechanistic link between BPNSs exposure and hepatocyte pyroptosis, emphasizing the efficacy of melatonin as a protective agent. It offers new insights for preventing BPNSs induced liver injury and provides a foundation for safer nanomaterial application strategies.</p>","PeriodicalId":22,"journal":{"name":"ACS Omega","volume":"9 47","pages":"46891-46903"},"PeriodicalIF":4.3000,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11603233/pdf/","citationCount":"0","resultStr":"{\"title\":\"Protective Role of Melatonin against Liver Toxicity from Black Phosphorus Nanosheets via Oxidative Stress and Pyroptosis.\",\"authors\":\"Bo Zhang, Yuechen Xing, Youtong Guo, Shuo Jin, Xinran Shao, Jiaqi Fan, Chunyi Zhang, Yue Wang\",\"doi\":\"10.1021/acsomega.4c05889\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>In the field of contemporary medicine, with the rapid application of nanomaterials, evaluating their biocompatibility and potential toxicity has become increasingly important. This study characterized black phosphorus nanosheets (BPNSs) and employed both in vivo and in vitro models to assess the impact of BPNSs exposure on oxidative stress and pyroptosis in hepatocytes. We investigated the hepatotoxicity of this emerging nanomaterial and the protective role of melatonin against BPNSs induced hepatocyte pyroptosis. The results showed that BPNSs exposure reduced hepatocyte viability, induced morphological changes, and elevated the expression of pyroptosis-related proteins, suggesting that BPNSs promote hepatocyte pyroptosis through the ROS-NLRP3-GSDMD pathway, thereby exacerbating the inflammatory response. Melatonin, a bioactive substance with anti-inflammatory and antioxidant properties, was found in our study to significantly mitigate these adverse effects. It emphasized the role of melatonin in regulating ROS production and related pathways, effectively protecting hepatocytes from BPNSs induced damage. This study elucidates the mechanistic link between BPNSs exposure and hepatocyte pyroptosis, emphasizing the efficacy of melatonin as a protective agent. It offers new insights for preventing BPNSs induced liver injury and provides a foundation for safer nanomaterial application strategies.</p>\",\"PeriodicalId\":22,\"journal\":{\"name\":\"ACS Omega\",\"volume\":\"9 47\",\"pages\":\"46891-46903\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2024-11-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11603233/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Omega\",\"FirstCategoryId\":\"92\",\"ListUrlMain\":\"https://doi.org/10.1021/acsomega.4c05889\",\"RegionNum\":3,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/11/26 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Omega","FirstCategoryId":"92","ListUrlMain":"https://doi.org/10.1021/acsomega.4c05889","RegionNum":3,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/26 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

摘要

在当代医学领域,随着纳米材料的快速应用,对其生物相容性和潜在毒性的评价变得越来越重要。本研究对黑磷纳米片(BPNSs)进行了表征,并采用体内和体外模型来评估BPNSs暴露对肝细胞氧化应激和焦亡的影响。我们研究了这种新兴纳米材料的肝毒性以及褪黑素对bpns诱导的肝细胞焦亡的保护作用。结果显示,BPNSs暴露可降低肝细胞活力,诱导形态学改变,升高肝细胞焦亡相关蛋白的表达,提示BPNSs通过ROS-NLRP3-GSDMD途径促进肝细胞焦亡,从而加重炎症反应。褪黑素是一种具有抗炎和抗氧化特性的生物活性物质,在我们的研究中发现,褪黑素可以显著减轻这些不良反应。强调褪黑素在调节ROS生成及相关通路中的作用,有效保护肝细胞免受BPNSs引起的损伤。本研究阐明了BPNSs暴露与肝细胞焦亡之间的机制联系,强调了褪黑激素作为保护剂的功效。这为预防BPNSs引起的肝损伤提供了新的见解,并为更安全的纳米材料应用策略提供了基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Role of Melatonin against Liver Toxicity from Black Phosphorus Nanosheets via Oxidative Stress and Pyroptosis.

In the field of contemporary medicine, with the rapid application of nanomaterials, evaluating their biocompatibility and potential toxicity has become increasingly important. This study characterized black phosphorus nanosheets (BPNSs) and employed both in vivo and in vitro models to assess the impact of BPNSs exposure on oxidative stress and pyroptosis in hepatocytes. We investigated the hepatotoxicity of this emerging nanomaterial and the protective role of melatonin against BPNSs induced hepatocyte pyroptosis. The results showed that BPNSs exposure reduced hepatocyte viability, induced morphological changes, and elevated the expression of pyroptosis-related proteins, suggesting that BPNSs promote hepatocyte pyroptosis through the ROS-NLRP3-GSDMD pathway, thereby exacerbating the inflammatory response. Melatonin, a bioactive substance with anti-inflammatory and antioxidant properties, was found in our study to significantly mitigate these adverse effects. It emphasized the role of melatonin in regulating ROS production and related pathways, effectively protecting hepatocytes from BPNSs induced damage. This study elucidates the mechanistic link between BPNSs exposure and hepatocyte pyroptosis, emphasizing the efficacy of melatonin as a protective agent. It offers new insights for preventing BPNSs induced liver injury and provides a foundation for safer nanomaterial application strategies.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
ACS Omega
ACS Omega Chemical Engineering-General Chemical Engineering
CiteScore
6.60
自引率
4.90%
发文量
3945
审稿时长
2.4 months
期刊介绍: ACS Omega is an open-access global publication for scientific articles that describe new findings in chemistry and interfacing areas of science, without any perceived evaluation of immediate impact.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信