• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法，用中文像聊天一样搜索，搜遍4000万医学文献。AI智能推荐，让科研检索更轻松。

立即免费搜索

文件翻译

保留排版，准确专业，支持PDF/Word/PPT等文件格式，支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述，25分钟生成高质量综述，智能提取关键信息，辅助科研写作。

立即免费体验

eNOS 对缺血后处理诱导的自噬在小鼠缺血/再灌注损伤中的作用。

Effect of eNOS on Ischemic Postconditioning-Induced Autophagy against Ischemia/Reperfusion Injury in Mice.

机构信息

Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210011, China.

Department of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, China.

出版信息

Biomed Res Int. 2019 Feb 10;2019:5201014. doi: 10.1155/2019/5201014. eCollection 2019.

DOI:10.1155/2019/5201014
PMID:30881990
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6387714/
Abstract

Autophagy is involved in the development of numerous illnesses, including ischemia/reperfusion (I/R). Endothelial nitric oxide synthase (eNOS) participates in the protective effects of ischemic postconditioning (IPostC). However, it remains unclear whether eNOS-mediated autophagy serves as a critical role in IPostC in the hearts of mice, in protecting against I/R injury. In the present study, the hearts of mice with left anterior descending coronary artery ligation were studied as I/R models. H9c2 cells underwent exposure to hypoxia/reoxygenation (H/R) and were examined as model. IPostC reduced mice myocardial infarct size and improved the structure of the heart. IPostC increased the formation of autophagosomes and increased the phosphorylation of eNOS and adenosine monophosphate-activated protein kinase (AMPK). Autophagy and eNOS inhibition suppressed the cardioprotective effects of IPostC. AMPK or eNOS inhibition abolished the improvement effect of IPostC on autophagy. AMPK inhibition decreased eNOS phosphorylation in the heart. Additionally, H9c2 cells suffering hypoxia were used as in vitro model. Autophagy or eNOS inhibition abolished the protective effects of hypoxic postconditioning (HPostC) against H/R injury. AMPK and eNOS inhibition/knockout decreased autophagic activity in the HPostC group. These results indicated that IPostC protects the heart against I/R injury, partially via promoting AMPK/eNOS-mediated autophagy.

摘要

自噬参与许多疾病的发展，包括缺血/再灌注（I/R）。内皮型一氧化氮合酶（eNOS）参与缺血后处理（IPostC）的保护作用。然而，eNOS 介导的自噬是否在保护小鼠心脏免受 I/R 损伤中发挥关键作用仍不清楚。在本研究中，结扎左前降支冠状动脉的小鼠心脏作为 I/R 模型进行研究。H9c2 细胞经历缺氧/复氧（H/R）作为模型进行检查。IPostC 减少了小鼠心肌梗死面积并改善了心脏结构。IPostC 增加了自噬体的形成，并增加了 eNOS 和单磷酸腺苷激活的蛋白激酶（AMPK）的磷酸化。自噬和 eNOS 抑制抑制了 IPostC 的心脏保护作用。AMPK 或 eNOS 抑制消除了 IPostC 对自噬的改善作用。AMPK 抑制降低了心脏中 eNOS 的磷酸化。此外，还使用缺氧的 H9c2 细胞作为体外模型。自噬或 eNOS 抑制消除了缺氧后处理（HPostC）对 H/R 损伤的保护作用。AMPK 和 eNOS 抑制/敲除降低了 HPostC 组的自噬活性。这些结果表明，IPostC 通过促进 AMPK/eNOS 介导的自噬来保护心脏免受 I/R 损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/2c8ff04a9850/BMRI2019-5201014.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/cb0adbf37a4a/BMRI2019-5201014.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/830b24d96120/BMRI2019-5201014.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/ba1750a61ba3/BMRI2019-5201014.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/de72d477ac8e/BMRI2019-5201014.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/e79a8e82ad22/BMRI2019-5201014.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/2c8ff04a9850/BMRI2019-5201014.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/cb0adbf37a4a/BMRI2019-5201014.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/830b24d96120/BMRI2019-5201014.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/ba1750a61ba3/BMRI2019-5201014.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/de72d477ac8e/BMRI2019-5201014.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/e79a8e82ad22/BMRI2019-5201014.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aea3/6387714/2c8ff04a9850/BMRI2019-5201014.006.jpg

相似文献

1
Effect of eNOS on Ischemic Postconditioning-Induced Autophagy against Ischemia/Reperfusion Injury in Mice.eNOS 对缺血后处理诱导的自噬在小鼠缺血/再灌注损伤中的作用。
Biomed Res Int. 2019 Feb 10;2019:5201014. doi: 10.1155/2019/5201014. eCollection 2019.
2
Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway.心肌缺血后处理通过激活nNOS/AMPK/mTOR通路促进自噬以对抗缺血再灌注损伤。
Int J Mol Sci. 2017 Mar 11;18(3):614. doi: 10.3390/ijms18030614.
3
Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.缺血后适应通过肌浆网和线粒体中的神经元型一氧化氮合酶保护心脏免受缺血再灌注损伤。
Cell Death Dis. 2016 May 12;7(5):e2222. doi: 10.1038/cddis.2016.108.
4
Ischemic postconditioning regulates cardiomyocyte autophagic activity following ischemia/reperfusion injury.缺血后处理可调节缺血/再灌注损伤后心肌细胞的自噬活性。
Mol Med Rep. 2015 Jul;12(1):1169-76. doi: 10.3892/mmr.2015.3533. Epub 2015 Mar 24.
5
DNA Hypomethylation of miR-30a Mediated the Protection of Hypoxia Postconditioning Against Aged Cardiomyocytes Hypoxia/Reoxygenation Injury Through Inhibiting Autophagy.miR-30a 的 DNA 低甲基化通过抑制自噬介导低氧后处理对衰老心肌细胞缺氧/复氧损伤的保护作用。
Circ J. 2020 Mar 25;84(4):616-625. doi: 10.1253/circj.CJ-19-0915. Epub 2020 Feb 29.
6
Ischemic postconditioning protects remodeled myocardium via the PI3K-PKB/Akt reperfusion injury salvage kinase pathway.缺血后适应通过PI3K-PKB/Akt再灌注损伤挽救激酶途径保护重塑心肌。
Cardiovasc Res. 2006 Oct 1;72(1):152-62. doi: 10.1016/j.cardiores.2006.06.027. Epub 2006 Jul 6.
7
rAAV9-Mediated MEK1 Gene Expression Restores Post-conditioning Protection Against Ischemia Injury in Hypertrophic Myocardium.rAAV9 介导的 MEK1 基因表达恢复肥厚心肌缺血后适应保护作用。
Cardiovasc Drugs Ther. 2020 Feb;34(1):3-14. doi: 10.1007/s10557-020-06936-8.
8
Effect of Ischemic Postconditioning on Myocardial Function and Infarct Size Following Reperfusion Injury in Diabetic Rats Pretreated With Vildagliptin.维格列汀预处理的糖尿病大鼠再灌注损伤后缺血后处理对心肌功能和梗死面积的影响
J Cardiovasc Pharmacol Ther. 2018 Mar;23(2):174-183. doi: 10.1177/1074248417729881. Epub 2017 Sep 13.
9
Hyperglycemia-Induced Overexpression of PH Domain Leucine-Rich Repeat Protein Phosphatase 1 (PHLPP1) Compromises the Cardioprotective Effect of Ischemic Postconditioning Via Modulation of the Akt/Mst1 Pathway Signaling.高血糖诱导的PH结构域富含亮氨酸重复蛋白磷酸酶1（PHLPP1）过表达通过调节Akt/Mst1信号通路损害缺血后处理的心脏保护作用。
Cardiovasc Drugs Ther. 2023 Dec;37(6):1087-1101. doi: 10.1007/s10557-022-07349-5. Epub 2022 Jun 18.
10
Selective inhibition of PTEN preserves ischaemic post-conditioning cardioprotection in STZ-induced Type 1 diabetic rats: role of the PI3K/Akt and JAK2/STAT3 pathways.选择性抑制PTEN可保留链脲佐菌素诱导的1型糖尿病大鼠缺血后处理的心脏保护作用：PI3K/Akt和JAK2/STAT3信号通路的作用
Clin Sci (Lond). 2016 Mar;130(5):377-92. doi: 10.1042/CS20150496. Epub 2015 Dec 14.

引用本文的文献

1
Clinical Applications for Gasotransmitters in the Cardiovascular System: Are We There Yet?气体信号分子在心血管系统中的临床应用：我们做到了吗？
Int J Mol Sci. 2023 Aug 5;24(15):12480. doi: 10.3390/ijms241512480.
2
Platelets and Cardioprotection: The Role of Nitric Oxide and Carbon Oxide.血小板与心脏保护：一氧化氮和一氧化碳的作用。
Int J Mol Sci. 2023 Mar 24;24(7):6107. doi: 10.3390/ijms24076107.
3
Myocardial injury: where inflammation and autophagy meet.心肌损伤：炎症与自噬的交汇之处

本文引用的文献

1
Development of a Long-Lived Luminescence Probe for Visualizing β-Galactosidase in Ovarian Carcinoma Cells.开发一种用于可视化卵巢癌细胞中β-半乳糖苷酶的长寿命荧光探针。
Anal Chem. 2017 Nov 7;89(21):11679-11684. doi: 10.1021/acs.analchem.7b03114. Epub 2017 Oct 12.
2
Postconditioning protects renal fibrosis by attenuating oxidative stress-induced mitochondrial injury.预处理通过减轻氧化应激诱导的线粒体损伤来保护肾纤维化。
Nephrol Dial Transplant. 2017 Oct 1;32(10):1628-1636. doi: 10.1093/ndt/gfw469.
3
Myocardial Ischemic Postconditioning Promotes Autophagy against Ischemia Reperfusion Injury via the Activation of the nNOS/AMPK/mTOR Pathway.
Burns Trauma. 2023 Mar 1;11:tkac062. doi: 10.1093/burnst/tkac062. eCollection 2023.
4
Role of AMPK in Myocardial Ischemia-Reperfusion Injury-Induced Cell Death in the Presence and Absence of Diabetes.在存在和不存在糖尿病的情况下，AMPK 在心肌缺血再灌注损伤诱导的细胞死亡中的作用。
Oxid Med Cell Longev. 2022 Oct 11;2022:7346699. doi: 10.1155/2022/7346699. eCollection 2022.
5
Oxidative Stress-Induced Growth Inhibitor (OSGIN1), a Target of X-Box-Binding Protein 1, Protects Palmitic Acid-Induced Vascular Lipotoxicity through Maintaining Autophagy.氧化应激诱导生长抑制剂1（OSGIN1）是X盒结合蛋白1的一个靶点，通过维持自噬保护棕榈酸诱导的血管脂毒性。
Biomedicines. 2022 Apr 25;10(5):992. doi: 10.3390/biomedicines10050992.
6
Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury.针对缺血再灌注损伤的心脏预处理策略中的线粒体质量控制
Life (Basel). 2021 Oct 21;11(11):1123. doi: 10.3390/life11111123.
7
New Insights in Molecular Mechanisms and Pathophysiology of Ischemia-Reperfusion Injury 2.0: An Updated Overview.缺血再灌注损伤的分子机制和病理生理学的新见解 2.0：更新概述。
Int J Mol Sci. 2020 Dec 22;22(1):28. doi: 10.3390/ijms22010028.
8
Involvement of HSP90 in ischemic postconditioning-induced cardioprotection by inhibition of the complement system, JNK and inflammation.热休克蛋白90通过抑制补体系统、JNK和炎症参与缺血后处理诱导的心脏保护作用。
Acta Cir Bras. 2020 Mar 20;35(1):e202000105. doi: 10.1590/s0102-865020200010000005. eCollection 2020.
9
Deferoxamine Treatment Combined With Sevoflurane Postconditioning Attenuates Myocardial Ischemia-Reperfusion Injury by Restoring HIF-1/BNIP3-Mediated Mitochondrial Autophagy in GK Rats.去铁胺治疗联合七氟醚后处理通过恢复GK大鼠中HIF-1/BNIP3介导的线粒体自噬减轻心肌缺血再灌注损伤
Front Pharmacol. 2020 Feb 19;11:6. doi: 10.3389/fphar.2020.00006. eCollection 2020.
心肌缺血后处理通过激活nNOS/AMPK/mTOR通路促进自噬以对抗缺血再灌注损伤。
Int J Mol Sci. 2017 Mar 11;18(3):614. doi: 10.3390/ijms18030614.
4
Over-expression of heat shock protein 70 protects mice against lung ischemia/reperfusion injury through SIRT1/AMPK/eNOS pathway.热休克蛋白70的过表达通过SIRT1/AMPK/eNOS途径保护小鼠免受肺缺血/再灌注损伤。
Am J Transl Res. 2016 Oct 15;8(10):4394-4404. eCollection 2016.
5
N-acetylcysteine attenuates myocardial dysfunction and postischemic injury by restoring caveolin-3/eNOS signaling in diabetic rats.N-乙酰半胱氨酸通过恢复糖尿病大鼠的小窝蛋白-3/内皮型一氧化氮合酶信号传导来减轻心肌功能障碍和缺血后损伤。
Cardiovasc Diabetol. 2016 Oct 12;15(1):146. doi: 10.1186/s12933-016-0460-z.
6
Measurement of Reactive Oxygen Species, Reactive Nitrogen Species, and Redox-Dependent Signaling in the Cardiovascular System: A Scientific Statement From the American Heart Association.心血管系统中活性氧、活性氮及氧化还原依赖性信号传导的测量：美国心脏协会科学声明
Circ Res. 2016 Aug 19;119(5):e39-75. doi: 10.1161/RES.0000000000000110. Epub 2016 Jul 14.
7
Effects of liraglutide and ischemic postconditioning on myocardial salvage after I/R injury in pigs.利拉鲁肽和缺血后处理对猪心肌缺血/再灌注损伤后心肌挽救的影响。
Scand Cardiovasc J. 2017 Feb;51(1):8-14. doi: 10.1080/14017431.2016.1197417. Epub 2016 Jul 5.
8
Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.缺血后适应通过肌浆网和线粒体中的神经元型一氧化氮合酶保护心脏免受缺血再灌注损伤。
Cell Death Dis. 2016 May 12;7(5):e2222. doi: 10.1038/cddis.2016.108.
9
Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner.艾塞那肽通过AMPK/Akt/eNOS途径以GLP-1受体依赖的方式对内皮细胞发挥直接保护作用。
Am J Physiol Endocrinol Metab. 2016 Jun 1;310(11):E947-57. doi: 10.1152/ajpendo.00400.2015. Epub 2016 Apr 12.
10
Combination of deep sea water and leaf extract prevents high-fat diet-induced obesity through AMPK activation in visceral adipose tissue.深海海水与树叶提取物的组合通过激活内脏脂肪组织中的AMPK来预防高脂饮食诱导的肥胖。
Exp Ther Med. 2016 Jan;11(1):338-344. doi: 10.3892/etm.2015.2852. Epub 2015 Nov 10.