右美托咪定通过调节缺氧诱导因子-1α减轻糖尿病大鼠心肌缺血/再灌注引起的急性肺损伤

IF 1.1 4区 医学 Q4 CARDIAC & CARDIOVASCULAR SYSTEMS
Siyu Chen, Jianjiang Wu, Long Yang, Taiwangu Tailaiti, T. Zou, Yidan Huan, Jiangyou Wang
{"title":"右美托咪定通过调节缺氧诱导因子-1α减轻糖尿病大鼠心肌缺血/再灌注引起的急性肺损伤","authors":"Siyu Chen, Jianjiang Wu, Long Yang, Taiwangu Tailaiti, T. Zou, Yidan Huan, Jiangyou Wang","doi":"10.21470/1678-9741-2020-0591","DOIUrl":null,"url":null,"abstract":"Introduction The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.","PeriodicalId":54481,"journal":{"name":"Revista Brasileira De Cirurgia Cardiovascular","volume":"37 1","pages":"370 - 379"},"PeriodicalIF":1.1000,"publicationDate":"2022-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α\",\"authors\":\"Siyu Chen, Jianjiang Wu, Long Yang, Taiwangu Tailaiti, T. Zou, Yidan Huan, Jiangyou Wang\",\"doi\":\"10.21470/1678-9741-2020-0591\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.\",\"PeriodicalId\":54481,\"journal\":{\"name\":\"Revista Brasileira De Cirurgia Cardiovascular\",\"volume\":\"37 1\",\"pages\":\"370 - 379\"},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2022-05-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Revista Brasileira De Cirurgia Cardiovascular\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.21470/1678-9741-2020-0591\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Revista Brasileira De Cirurgia Cardiovascular","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21470/1678-9741-2020-0591","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 2

摘要

引言本研究旨在探讨右美托咪定(Dex)通过抑制缺氧诱导因子-1α(HIF-1α)对糖尿病大鼠心肌缺血/再灌注(MIR)诱导的急性肺损伤(ALI)的保护作用机制。方法健康雄性Sprague-Dawley大鼠先用链脲佐菌素诱导糖尿病。然后,在诱导后三周,在MIR建模前30分钟将Dex或慢病毒载体(LV)-HIF-1α注射到大鼠中。4周后,采集肺组织用于病理变化观察和湿/干重(W/D)比测定。之后,测量氧化应激指标和促炎因子。此外,通过免疫组织化学和蛋白质印迹分析评估HIF-1α的表达。结果地塞米松能抑制炎症细胞浸润,改善肺组织结构,降低病理评分和W/D比,阻断氧化应激和炎症反应。此外,Dex还能抑制HIF-1α的表达。此外,Dex+LV-HIF-1α逆转了Dex对糖尿病MIR诱导的ALI的保护作用。结论Dex在糖尿病MIR诱导的ALI中抑制HIF-1α的上调,从而通过抑制氧自由基的积累和减轻肺部炎症反应来保护肺功能。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Dexmedetomidine Leads to the Mitigation of Myocardial Ischemia/Reperfusion-Induced Acute Lung Injury in Diabetic Rats Via Modulation of Hypoxia-Inducible Factor-1α
Introduction The objective of this study is to investigate the protective mechanism of dexmedetomidine (Dex) in myocardial ischemia/reperfusion (MIR)-induced acute lung injury (ALI) of diabetic rats by inhibiting hypoxia-inducible factor-1α (HIF-1α). Methods Initially, healthy male Sprague Dawley rats were treated with streptozocin to induce diabetes. Then, three weeks after the induction, Dex or lentiviral vector (LV)-HIF-1α was injected into the rats 30 minutes prior to the MIR modeling. After four weeks, lung tissues were harvested for pathological changes observation and the wet/dry weight (W/D) ratio determination. Afterwards, oxidative stress indicators and pro-inflammatory factors were measured. In addition, HIF-1α expression was assessed by immunohistochemistry and western blot analysis. Results Dex could suppress inflammatory cell infiltration, improve lung tissue structure, reduce pathological score and the W/D ratio, and block oxidative stress and inflammatory response in MIR-induced ALI of diabetic rats. Besides, Dex could also inhibit HIF-1α expression. Moreover, Dex + LV-HIF-1α reversed the protective role of Dex on diabetic MIR-induced ALI. Conclusion Our study has made it clear that Dex inhibited the upregulation of HIF-1α in diabetic MIR-induced ALI, and thus protect lung functions by quenching the accumulation of oxygen radical and reducing lung inflammatory response.
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
Revista Brasileira De Cirurgia Cardiovascular
Revista Brasileira De Cirurgia Cardiovascular CARDIAC & CARDIOVASCULAR SYSTEMS-SURGERY
CiteScore
2.10
自引率
0.00%
发文量
176
审稿时长
20 weeks
期刊介绍: Brazilian Journal of Cardiovascular Surgery (BJCVS) is the official journal of the Brazilian Society of Cardiovascular Surgery (SBCCV). BJCVS is a bimonthly, peer-reviewed scientific journal, with regular circulation since 1986. BJCVS aims to record the scientific and innovation production in cardiovascular surgery and promote study, improvement and professional updating in the specialty. It has significant impact on cardiovascular surgery practice and related areas.
×
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:481959085
Book学术官方微信