Nitric Oxide/Glucose Transporter Type 4 Pathway Mediates Cardioprotection against Ischemia/Reperfusion Injury under Hyperglycemic and Diabetic Conditions in Rats.

IF 1.8 4区 医学 Q3 PERIPHERAL VASCULAR DISEASE
Journal of Vascular Research Pub Date : 2024-01-01 Epub Date: 2024-06-28 DOI:10.1159/000539461
Aisha Al-Kouh, Fawzi Babiker
{"title":"Nitric Oxide/Glucose Transporter Type 4 Pathway Mediates Cardioprotection against Ischemia/Reperfusion Injury under Hyperglycemic and Diabetic Conditions in Rats.","authors":"Aisha Al-Kouh, Fawzi Babiker","doi":"10.1159/000539461","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>The comorbidities of ischemic heart disease (IHD) and diabetes mellitus (DM) compromise the protection of the diabetic heart from ischemia/reperfusion (I/R) injury. We hypothesized that manipulation of reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways might protect the diabetic heart, and intervention of these pathways could be a new avenue for potentially protecting the diabetic heart.</p><p><strong>Methods: </strong>All hearts were subjected to 30-min ischemia and 30-min reperfusion. During reperfusion, hearts were exposed to molecules proven to protect the heart from I/R injury. The hemodynamic data were collected using suitable software. The infarct size, troponin T levels, and protein levels in hearts were evaluated.</p><p><strong>Results: </strong>Both cyclosporine-A and nitric oxide donor (SNAP) infusion at reperfusion protected 4-week diabetic hearts from I/R injury. However, 6-week diabetic hearts were protected only by SNAP, but not cyclosporin-A. These treatments significantly (p &lt; 0.05) improved cardiac hemodynamics and decreased infarct size.</p><p><strong>Conclusions: </strong>The administration of SNAP to diabetic hearts protected both 4- and 6-week diabetic hearts; however, cyclosporine-A protected only the 4-week diabetic hearts. The eNOS/GLUT-4 pathway executed the SNAP-mediated cardioprotection.</p>","PeriodicalId":17530,"journal":{"name":"Journal of Vascular Research","volume":" ","pages":"179-196"},"PeriodicalIF":1.8000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Vascular Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000539461","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/6/28 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: The comorbidities of ischemic heart disease (IHD) and diabetes mellitus (DM) compromise the protection of the diabetic heart from ischemia/reperfusion (I/R) injury. We hypothesized that manipulation of reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways might protect the diabetic heart, and intervention of these pathways could be a new avenue for potentially protecting the diabetic heart.

Methods: All hearts were subjected to 30-min ischemia and 30-min reperfusion. During reperfusion, hearts were exposed to molecules proven to protect the heart from I/R injury. The hemodynamic data were collected using suitable software. The infarct size, troponin T levels, and protein levels in hearts were evaluated.

Results: Both cyclosporine-A and nitric oxide donor (SNAP) infusion at reperfusion protected 4-week diabetic hearts from I/R injury. However, 6-week diabetic hearts were protected only by SNAP, but not cyclosporin-A. These treatments significantly (p < 0.05) improved cardiac hemodynamics and decreased infarct size.

Conclusions: The administration of SNAP to diabetic hearts protected both 4- and 6-week diabetic hearts; however, cyclosporine-A protected only the 4-week diabetic hearts. The eNOS/GLUT-4 pathway executed the SNAP-mediated cardioprotection.

一氧化氮/葡萄糖转运体 4 型通路介导大鼠在高血糖和糖尿病条件下对缺血/再灌注损伤的心脏保护作用
导言:缺血性心脏病(IHD)和糖尿病(DM)的合并症损害了糖尿病心脏对缺血/再灌注(I/R)损伤的保护。我们假设,操纵再灌注损伤挽救激酶(RISK)和幸存者激活因子增强(SAFE)通路可能会保护糖尿病心脏,对这些通路的干预可能是保护糖尿病心脏的新途径:方法:对所有心脏进行 30 分钟缺血和 30 分钟再灌注。方法:对所有心脏进行 30 分钟缺血和 30 分钟再灌注,在再灌注期间,心脏暴露于经证实能保护心脏免受 I/R 损伤的分子。使用合适的软件收集血液动力学数据。结果显示,环孢素-A和硝酸甘油都能保护心脏免受I/R损伤:结果:环孢素-A 和一氧化氮供体(SNAP)在再灌注时都能保护 4 周糖尿病患者的心脏免受 I/R 损伤。然而,6周糖尿病患者的心脏只受到SNAP的保护,而没有受到环孢素-A的保护。这些治疗方法能明显(p < 0.05)改善心脏血流动力学并缩小梗死面积:结论:对糖尿病心脏施用 SNAP 可保护 4 周和 6 周糖尿病心脏;但环孢素-A 只保护 4 周糖尿病心脏。eNOS/GLUT-4通路发挥了SNAP介导的心脏保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Vascular Research
Journal of Vascular Research 医学-生理学
CiteScore
3.40
自引率
0.00%
发文量
25
审稿时长
>12 weeks
期刊介绍: The ''Journal of Vascular Research'' publishes original articles and reviews of scientific excellence in vascular and microvascular biology, physiology and pathophysiology. The scope of the journal covers a broad spectrum of vascular and lymphatic research, including vascular structure, vascular function, haemodynamics, mechanics, cell signalling, intercellular communication, growth and differentiation. JVR''s ''Vascular Update'' series regularly presents state-of-the-art reviews on hot topics in vascular biology. Manuscript processing times are, consistent with stringent review, kept as short as possible due to electronic submission. All articles are published online first, ensuring rapid publication. The ''Journal of Vascular Research'' is the official journal of the European Society for Microcirculation. A biennial prize is awarded to the authors of the best paper published in the journal over the previous two years, thus encouraging young scientists working in the exciting field of vascular biology to publish their findings.
×
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