• 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

比较化学缺氧和物理缺氧诱导的心肌细胞缺氧效应。

Comparison of hypoxic effects induced by chemical and physical hypoxia on cardiomyocytes.

机构信息

Department of Aerospace Physiology, Fourth Military Medical University, Key Laboratory of Aerospace Medicine, Ministry of China, Xi'an 710032, China.

出版信息

Can J Physiol Pharmacol. 2019 Oct;97(10):980-988. doi: 10.1139/cjpp-2019-0092. Epub 2019 May 28.

DOI:10.1139/cjpp-2019-0092
PMID:31136722
Abstract

The degree and duration of chemical hypoxia induced by sodium dithionite (NaSO) have not been reported. It is not yet clear how much reduction in the O concentration (physical hypoxia) can lead to hypoxia in cultured cardiomyocytes. In this study, oxygen microelectrodes were used to measure changes in the O concentration in media containing different concentrations of NaSO. Then, hypoxic effects of 0.8, 1.0, and 2.0 mM NaSO or 1%, 3%, and 5% O in cultured cardiomyocytes from neonatal rats were observed and compared. The results showed that the O concentration failed to remain constant by NaSO treatment during the 180-minute observation period. Only the 2.0 mM NaSO group significantly increased the expression of hypoxia-inducible factor 1α (HIF-1α) and hypoxic responses. Notably, 3% O only significantly increased the expression of HIF-1α in cardiomyocytes, while 1% O not only increased the expression of HIF-1α but also increased the apoptotic rate in cardiomyocytes. These results suggest that NaSO is not suitable for establishing a hypoxic model in cultured neonatal rat cardiomyocytes, and neonatal rat cardiomyocytes cultured at or below 1% O induced significant hypoxic effects, which can be used as a starting O concentration for establishing a hypoxic cell model.

摘要

连二亚硫酸钠(NaSO)诱导的化学缺氧程度和持续时间尚未报道。目前尚不清楚氧浓度(物理缺氧)降低多少会导致培养的心肌细胞缺氧。在这项研究中,使用氧微电极测量了含有不同浓度 NaSO 的培养基中氧浓度的变化。然后,观察并比较了 0.8、1.0 和 2.0mM NaSO 或 1%、3%和 5%O 对新生大鼠心肌细胞的缺氧作用。结果表明,在 180 分钟的观察期内,NaSO 处理未能使氧浓度保持恒定。只有 2.0mM NaSO 组显著增加了缺氧诱导因子 1α(HIF-1α)的表达和缺氧反应。值得注意的是,3%O 仅显著增加了心肌细胞中 HIF-1α 的表达,而 1%O 不仅增加了 HIF-1α 的表达,还增加了心肌细胞的凋亡率。这些结果表明,NaSO 不适合用于建立培养的新生大鼠心肌细胞缺氧模型,并且培养在 1%O 或更低水平的新生大鼠心肌细胞会引起明显的缺氧作用,可作为建立缺氧细胞模型的起始氧浓度。

相似文献

1
Comparison of hypoxic effects induced by chemical and physical hypoxia on cardiomyocytes.比较化学缺氧和物理缺氧诱导的心肌细胞缺氧效应。
Can J Physiol Pharmacol. 2019 Oct;97(10):980-988. doi: 10.1139/cjpp-2019-0092. Epub 2019 May 28.
2
[Role of hypoxia-inducible factor-1alpha in the prevention of cardiomyocyte injury induced by hypoxic preconditioning].[缺氧诱导因子-1α在缺氧预处理预防心肌细胞损伤中的作用]
Sheng Li Xue Bao. 2004 Oct 25;56(5):609-14.
3
[Changes in expression of apoptosis correlative proteins and HIF-1 during acute hypoxia and hypoxic preconditioning in cultured cardiomyocyte of rat].
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2005 Nov;21(4):423-6.
4
Effect of hypoxia-inducible factor 1-alpha on hypoxia/reoxygenation-induced apoptosis in primary neonatal rat cardiomyocytes.缺氧诱导因子 1-α对原代新生大鼠心肌细胞缺氧/复氧诱导凋亡的影响。
Biochem Biophys Res Commun. 2012 Jan 27;417(4):1227-34. doi: 10.1016/j.bbrc.2011.12.115. Epub 2011 Dec 29.
5
Microtubular stability affects cardiomyocyte glycolysis by HIF-1alpha expression and endonuclear aggregation during early stages of hypoxia.微管稳定性通过低氧早期 HIF-1alpha 表达和核内聚集影响心肌细胞糖酵解。
Am J Physiol Heart Circ Physiol. 2010 Jun;298(6):H1919-31. doi: 10.1152/ajpheart.01039.2009. Epub 2010 Mar 12.
6
[Protective effects and mechanism of keratinocyte growth factor combined with hypoxia inducible factor-1α on intestinal crypt epithelial cells of rats with hypoxia stress].角质形成细胞生长因子联合缺氧诱导因子-1α对缺氧应激大鼠肠隐窝上皮细胞的保护作用及机制
Zhonghua Shao Shang Za Zhi. 2019 Jan 20;35(1):54-61. doi: 10.3760/cma.j.issn.1009-2587.2019.01.010.
7
The effect of hypoxia-inducible factor 1-alpha on hypoxia-induced apoptosis in primary neonatal rat ventricular myocytes.缺氧诱导因子1-α对原代新生大鼠心室肌细胞缺氧诱导凋亡的影响。
Cardiovasc J Afr. 2010 Jan-Feb;21(1):37-41.
8
Mechanism of TNF-α autocrine effects in hypoxic cardiomyocytes: initiated by hypoxia inducible factor 1α, presented by exosomes.缺氧心肌细胞中 TNF-α 自分泌作用的机制:由缺氧诱导因子 1α 启动,由外泌体呈现。
J Mol Cell Cardiol. 2012 Dec;53(6):848-57. doi: 10.1016/j.yjmcc.2012.10.002. Epub 2012 Oct 16.
9
[Inhibition of the expression of cardiomyocytic hypoxic induction factor-1alpha during hypoxic state by double chain siRNA].双链小干扰RNA对缺氧状态下心肌细胞缺氧诱导因子-1α表达的抑制作用
Zhonghua Shao Shang Za Zhi. 2004 Oct;20(5):278-80.
10
Hypoxia suppresses myocardial survival pathway through HIF-1α-IGFBP-3-dependent signaling and enhances cardiomyocyte autophagic and apoptotic effects mainly via FoxO3a-induced BNIP3 expression.缺氧通过HIF-1α-IGFBP-3依赖性信号传导抑制心肌存活途径,并主要通过FoxO3a诱导的BNIP3表达增强心肌细胞自噬和凋亡作用。
Growth Factors. 2016 Aug;34(3-4):73-86. doi: 10.1080/08977194.2016.1191480. Epub 2016 Jul 1.

引用本文的文献

1
The role of atropine in myopia control: insights into choroidal and scleral mechanisms.阿托品在近视控制中的作用:对脉络膜和巩膜机制的见解。
Front Pharmacol. 2025 Mar 20;16:1509196. doi: 10.3389/fphar.2025.1509196. eCollection 2025.
2
Cytoprotective Action of Sodium Fumarate in an Model of Hypoxia Using Sodium Dithionite.连二亚硫酸钠诱导的缺氧模型中富马酸钠的细胞保护作用
Sovrem Tekhnologii Med. 2025;17(1):93-106. doi: 10.17691/stm2025.17.1.09. Epub 2025 Feb 28.
3
Withaferin A Enhances Mitochondrial Biogenesis and BNIP3-Mediated Mitophagy to Promote Rapid Adaptation to Extreme Hypoxia.
醉茄素 A 通过促进线粒体生物发生和 BNIP3 介导的自噬来促进快速适应极端缺氧。
Cells. 2022 Dec 25;12(1):85. doi: 10.3390/cells12010085.
4
Proteasome Inhibitors Decrease the Viability of Pulmonary Arterial Smooth Muscle Cells by Restoring Mitofusin-2 Expression under Hypoxic Conditions.蛋白酶体抑制剂通过在缺氧条件下恢复线粒体融合蛋白2的表达来降低肺动脉平滑肌细胞的活力。
Biomedicines. 2022 Apr 9;10(4):873. doi: 10.3390/biomedicines10040873.
5
Engineering the Cellular Microenvironment of Post-infarct Myocardium on a Chip.在芯片上构建心肌梗死后心肌的细胞微环境
Front Cardiovasc Med. 2021 Jul 14;8:709871. doi: 10.3389/fcvm.2021.709871. eCollection 2021.