丹参素甲酯通过抑制 TLR4/NF-κB 通路减轻 LPS 诱导的急性肺损伤

IF 1.9 4区 医学 Q3 PHYSIOLOGY Respiratory Physiology & Neurobiology Pub Date : 2024-01-18 DOI:10.1016/j.resp.2024.104219
Xuejia Han , Wensi Ding , Guiwu Qu , Youjie Li , Pingyu Wang , Jiahui Yu , Mingyue Liu , Xiulan Chen , Shuyang Xie , Jiankai Feng , Sen Xu
{"title":"丹参素甲酯通过抑制 TLR4/NF-κB 通路减轻 LPS 诱导的急性肺损伤","authors":"Xuejia Han ,&nbsp;Wensi Ding ,&nbsp;Guiwu Qu ,&nbsp;Youjie Li ,&nbsp;Pingyu Wang ,&nbsp;Jiahui Yu ,&nbsp;Mingyue Liu ,&nbsp;Xiulan Chen ,&nbsp;Shuyang Xie ,&nbsp;Jiankai Feng ,&nbsp;Sen Xu","doi":"10.1016/j.resp.2024.104219","DOIUrl":null,"url":null,"abstract":"<div><p><span><span>Acute Lung Injury (ALI) manifests as an acute exacerbation of pulmonary inflammation with high mortality. The potential application of </span>Danshensu<span><span><span><span> methyl ester (DME, synthesized in our lab) in ameliorating ALI has not been elucidated. Our results demonstrated that DME led to a remarkable reduction in lung injury. DME promoted a marked increase in </span>antioxidant enzymes, like </span>superoxide dismutase<span> (SOD), and glutathione<span> (GSH), accompanied by a substantial decrease in reactive oxygen species<span> (ROS), myeloperoxidase (MPO), and </span></span></span></span>malondialdehyde (MDA). Moreover, DME decreased the production of IL-1β, TNF-α and IL-6, </span></span><em>in vitro</em> and <em>in vivo</em><span>. TLR4<span> and MyD88 expression is reduced in the DME-treated cells or tissues, which further leading to a decrease of p-p65 and p-IκBα. Meanwhile, DME effectively facilitated an elevation in cytoplasmic p65 expression. In summary, DME could ameliorate ALI by its antioxidant functionality and anti-inflammation effects through TLR4/NF-κB, which implied that DME may be a viable medicine for lung injury.</span></span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Danshensu methyl ester attenuated LPS-induced acute lung injury by inhibiting TLR4/NF-κB pathway\",\"authors\":\"Xuejia Han ,&nbsp;Wensi Ding ,&nbsp;Guiwu Qu ,&nbsp;Youjie Li ,&nbsp;Pingyu Wang ,&nbsp;Jiahui Yu ,&nbsp;Mingyue Liu ,&nbsp;Xiulan Chen ,&nbsp;Shuyang Xie ,&nbsp;Jiankai Feng ,&nbsp;Sen Xu\",\"doi\":\"10.1016/j.resp.2024.104219\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span><span>Acute Lung Injury (ALI) manifests as an acute exacerbation of pulmonary inflammation with high mortality. The potential application of </span>Danshensu<span><span><span><span> methyl ester (DME, synthesized in our lab) in ameliorating ALI has not been elucidated. Our results demonstrated that DME led to a remarkable reduction in lung injury. DME promoted a marked increase in </span>antioxidant enzymes, like </span>superoxide dismutase<span> (SOD), and glutathione<span> (GSH), accompanied by a substantial decrease in reactive oxygen species<span> (ROS), myeloperoxidase (MPO), and </span></span></span></span>malondialdehyde (MDA). Moreover, DME decreased the production of IL-1β, TNF-α and IL-6, </span></span><em>in vitro</em> and <em>in vivo</em><span>. TLR4<span> and MyD88 expression is reduced in the DME-treated cells or tissues, which further leading to a decrease of p-p65 and p-IκBα. Meanwhile, DME effectively facilitated an elevation in cytoplasmic p65 expression. In summary, DME could ameliorate ALI by its antioxidant functionality and anti-inflammation effects through TLR4/NF-κB, which implied that DME may be a viable medicine for lung injury.</span></span></p></div>\",\"PeriodicalId\":20961,\"journal\":{\"name\":\"Respiratory Physiology & Neurobiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2024-01-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Respiratory Physiology & Neurobiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1569904824000120\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Respiratory Physiology & Neurobiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1569904824000120","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

急性肺损伤(ALI)表现为肺部炎症的急性加重,死亡率很高。丹参素甲酯(DME,由我们实验室合成)在改善急性肺损伤方面的潜在应用尚未阐明。我们的研究结果表明,丹参素甲酯能显著减轻肺损伤。DME促进了超氧化物歧化酶(SOD)和谷胱甘肽(GSH)等抗氧化酶的明显增加,同时大幅减少了活性氧(ROS)、髓过氧化物酶(MPO)和丙二醛(MDA)。此外,DME 还能减少体外和体内 IL-1β、TNF-α 和 IL-6 的产生。TLR4和MyD88在经DME处理的细胞或组织中的表达减少,从而进一步导致p-p65和p-IκBα的减少。同时,DME能有效促进细胞质p65表达的增加。综上所述,二甲双胍可通过其抗氧化功能和TLR4/NF-κB的抗炎作用改善ALI,这意味着二甲双胍可能是一种治疗肺损伤的可行药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Danshensu methyl ester attenuated LPS-induced acute lung injury by inhibiting TLR4/NF-κB pathway

Acute Lung Injury (ALI) manifests as an acute exacerbation of pulmonary inflammation with high mortality. The potential application of Danshensu methyl ester (DME, synthesized in our lab) in ameliorating ALI has not been elucidated. Our results demonstrated that DME led to a remarkable reduction in lung injury. DME promoted a marked increase in antioxidant enzymes, like superoxide dismutase (SOD), and glutathione (GSH), accompanied by a substantial decrease in reactive oxygen species (ROS), myeloperoxidase (MPO), and malondialdehyde (MDA). Moreover, DME decreased the production of IL-1β, TNF-α and IL-6, in vitro and in vivo. TLR4 and MyD88 expression is reduced in the DME-treated cells or tissues, which further leading to a decrease of p-p65 and p-IκBα. Meanwhile, DME effectively facilitated an elevation in cytoplasmic p65 expression. In summary, DME could ameliorate ALI by its antioxidant functionality and anti-inflammation effects through TLR4/NF-κB, which implied that DME may be a viable medicine for lung injury.

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
CiteScore
4.80
自引率
8.70%
发文量
104
审稿时长
54 days
期刊介绍: Respiratory Physiology & Neurobiology (RESPNB) publishes original articles and invited reviews concerning physiology and pathophysiology of respiration in its broadest sense. Although a special focus is on topics in neurobiology, high quality papers in respiratory molecular and cellular biology are also welcome, as are high-quality papers in traditional areas, such as: -Mechanics of breathing- Gas exchange and acid-base balance- Respiration at rest and exercise- Respiration in unusual conditions, like high or low pressure or changes of temperature, low ambient oxygen- Embryonic and adult respiration- Comparative respiratory physiology. Papers on clinical aspects, original methods, as well as theoretical papers are also considered as long as they foster the understanding of respiratory physiology and pathophysiology.
期刊最新文献
Endomorphin-2 (Endo2) and substance P (SubP) co-application attenuates SubP-induced excitation and alters frequency plasticity in neonatal rat in vitro preparations Lateral hypothalamic astrocytes contribute to the hypercapnic chemoreflex in a light-dark cycle-dependent manner in unanesthetized rats The acute effect of respiratory muscle training on cortisol, testosterone, and testosterone-to-cortisol ratio in well-trained triathletes - exploratory study Ticagrelor-related dyspnea beyond adenosine: Insights into retrotrapezoid hyperactivity 4-Hydroxychalcone attenuates ovalbumin-induced allergic airway inflammation and oxidative stress by activating Nrf2/GPx4 pathway
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1