• 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

Thiamine attenuates hypoxia-induced cell death in cultured neonatal rat cardiomyocytes.

作者信息

Shin Bo Hee, Choi Seung Hyuk, Cho Eun Young, Shin Min-Jeong, Hwang Ki-Chul, Cho Hong Keun, Chung Ji Hyung, Jang Yangsoo

机构信息

Cardiovascular Research Institute, Yonsei University College of Medicine, Seoul 120-752, Korea.

出版信息

Mol Cells. 2004 Oct 31;18(2):133-40.

PMID:15528987
Abstract

Previous studies have demonstrated that thiamine (vitamin B1) has a cytoprotective effect against ischemic damage to the heart, and that heat shock protein 70 (Hsp70) is capable of protecting cardiac cells from lethal ischemia/hypoxia. We show here that thiamine has a cytoprotective effect on cultured neonatal rat cardiomyocytes under hypoxic insult, and also protects the cardiomyocytes against hypoxia-induced apoptosis; caspase-3 activation, PARP cleavage and DNA fragmentation are all inhibited. Moreover, it increases the level of Hsp70 protein in the cardiomyocytes even under prolonged hypoxic stress and its effects on hypoxia-induced cardiac cell death are antagonized by an Hsp70 inhibitor. These results suggest that the cytoprotective effect of thiamine in cardiomyocytes under hypoxic stress is due to its ability to induce Hsp70.

摘要

相似文献

1
Thiamine attenuates hypoxia-induced cell death in cultured neonatal rat cardiomyocytes.
Mol Cells. 2004 Oct 31;18(2):133-40.
2
Hsp70 attenuates hypoxia/reoxygenation-induced activation of poly(ADP-ribose) synthetase in the nucleus of adult rat cardiomyocytes.热休克蛋白70减轻成年大鼠心肌细胞核中缺氧/复氧诱导的聚(ADP-核糖)合成酶的激活。
Mol Cell Biochem. 2003 Jun;248(1-2):149-55. doi: 10.1023/a:1024192403758.
3
Heat shock pretreatment inhibited the release of Smac/DIABLO from mitochondria and apoptosis induced by hydrogen peroxide in cardiomyocytes and C2C12 myogenic cells.热休克预处理抑制了心肌细胞和C2C12成肌细胞中线粒体Smac/DIABLO的释放以及过氧化氢诱导的细胞凋亡。
Cell Stress Chaperones. 2005 Autumn;10(3):252-62. doi: 10.1379/csc-124r.1.
4
Ischemic preconditioning attenuates ischemia/reperfusion-induced activation of caspases and subsequent cleavage of poly(ADP-ribose) polymerase in rat hearts in vivo.缺血预处理可减轻体内大鼠心脏缺血/再灌注诱导的半胱天冬酶激活及随后的聚(ADP - 核糖)聚合酶裂解。
Cardiovasc Res. 1999 Dec;44(3):536-42. doi: 10.1016/s0008-6363(99)00227-8.
5
Ozone protects cardiomyocytes against ischemia/reperfusion injury: Regulating the heat shock protein 70 (HPS70) expression through activating the JAK2/STAT3 Pathway.臭氧保护心肌细胞免受缺血/再灌注损伤:通过激活 JAK2/STAT3 通路调节热休克蛋白 70(HSP70)的表达。
Bioengineered. 2021 Dec;12(1):6606-6616. doi: 10.1080/21655979.2021.1974760.
6
AMP-activated protein kinase protects cardiomyocytes against hypoxic injury through attenuation of endoplasmic reticulum stress.AMP激活的蛋白激酶通过减轻内质网应激来保护心肌细胞免受缺氧损伤。
Mol Cell Biol. 2005 Nov;25(21):9554-75. doi: 10.1128/MCB.25.21.9554-9575.2005.
7
Phenylephrine protects neonatal rat cardiomyocytes from hypoxia and serum deprivation-induced apoptosis.去氧肾上腺素可保护新生大鼠心肌细胞免受缺氧和血清剥夺诱导的细胞凋亡。
Cell Death Differ. 2000 Sep;7(9):773-84. doi: 10.1038/sj.cdd.4400721.
8
MicroRNA-223 protects neonatal rat cardiomyocytes and H9c2 cells from hypoxia-induced apoptosis and excessive autophagy via the Akt/mTOR pathway by targeting PARP-1.miR-223 通过靶向 PARP-1 保护新生大鼠心肌细胞和 H9c2 细胞免于缺氧诱导的凋亡和过度自噬,通过 Akt/mTOR 通路。
J Mol Cell Cardiol. 2018 May;118:133-146. doi: 10.1016/j.yjmcc.2018.03.018. Epub 2018 Mar 31.
9
ERKs/p53 signal transduction pathway is involved in doxorubicin-induced apoptosis in H9c2 cells and cardiomyocytes.细胞外调节蛋白激酶/ p53信号转导通路参与阿霉素诱导的H9c2细胞和心肌细胞凋亡。
Am J Physiol Heart Circ Physiol. 2008 Nov;295(5):H1956-65. doi: 10.1152/ajpheart.00407.2008. Epub 2008 Sep 5.
10
EMF protects cardiomyocytes against hypoxia-induced injury via heat shock protein 70 activation.电磁场通过激活热休克蛋白70保护心肌细胞免受缺氧诱导的损伤。
Chem Biol Interact. 2016 Mar 25;248:8-17. doi: 10.1016/j.cbi.2016.02.003. Epub 2016 Feb 11.

引用本文的文献

1
Thiamine (Vitamin B1)-An Essential Health Regulator.硫胺素(维生素B1)——一种必需的健康调节剂。
Nutrients. 2025 Jul 2;17(13):2206. doi: 10.3390/nu17132206.
2
Protective Role of Vitamin B in Doxorubicin-Induced Cardiotoxicity in Rats: Focus on Hemodynamic, Redox, and Apoptotic Markers in Heart.维生素B在阿霉素诱导的大鼠心脏毒性中的保护作用:聚焦于心脏的血流动力学、氧化还原和凋亡标志物
Front Physiol. 2021 Sep 22;12:690619. doi: 10.3389/fphys.2021.690619. eCollection 2021.
3
Implications of venous thromboembolism GWAS reported genetic makeup in the clinical outcome of ovarian cancer patients.
静脉血栓栓塞症 GWAS 报道的遗传构成与卵巢癌患者的临床结局相关。
Pharmacogenomics J. 2021 Apr;21(2):222-232. doi: 10.1038/s41397-020-00201-9. Epub 2020 Nov 7.
4
Role of HIF-1α in the hypoxia inducible expression of the thiamine transporter, SLC19A3.低氧诱导因子-1α(HIF-1α)在硫胺素转运体SLC19A3低氧诱导表达中的作用
Gene. 2016 Dec 31;595(2):212-220. doi: 10.1016/j.gene.2016.10.013. Epub 2016 Oct 12.
5
Affective brain areas and sleep-disordered breathing.情感脑区与睡眠呼吸障碍
Prog Brain Res. 2014;209:275-93. doi: 10.1016/B978-0-444-63274-6.00014-X.
6
Linking vitamin B1 with cancer cell metabolism.将维生素 B1 与癌细胞代谢联系起来。
Cancer Metab. 2013 Jul 24;1(1):16. doi: 10.1186/2049-3002-1-16.
7
Role of thiamine in Alzheimer's disease.硫胺素在阿尔茨海默病中的作用。
Am J Alzheimers Dis Other Demen. 2011 Dec;26(8):588-98. doi: 10.1177/1533317511432736. Epub 2012 Jan 4.
8
Brain axonal and myelin evaluation in heart failure.心力衰竭患者的脑轴突和髓鞘评估。
J Neurol Sci. 2011 Aug 15;307(1-2):106-13. doi: 10.1016/j.jns.2011.04.028. Epub 2011 May 25.
9
Global and regional putamen volume loss in patients with heart failure.心力衰竭患者的全球和区域性壳核体积损失。
Eur J Heart Fail. 2011 Jun;13(6):651-5. doi: 10.1093/eurjhf/hfr012. Epub 2011 Mar 9.
10
Thiamine status in humans and content of phosphorylated thiamine derivatives in biopsies and cultured cells.人体中硫胺素的状态和活检组织及培养细胞中磷酸化硫胺素衍生物的含量。
PLoS One. 2010 Oct 25;5(10):e13616. doi: 10.1371/journal.pone.0013616.