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葛根素通过下调电压依赖性阴离子通道1（VDAC1）抑制铁死亡，从而保护心肌免受缺血/再灌注损伤。

Puerarin Protects Myocardium From Ischaemia/Reperfusion Injury by Inhibiting Ferroptosis Through Downregulation of VDAC1.

作者信息

Hu Fajia, Hu Tie, He Andi, Yuan Yong, Wang Xiuqi, Zou Chenchao, Qiao Yamei, Xu Huaihan, Liu Lanxiang, Wang Qun, Liu Jichun, Lai Songqing, Huang Huang

机构信息

Institute of Cardiovascular Surgical Diseases, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.

Department of Cardiovascular Surgery, the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.

出版信息

J Cell Mol Med. 2024 Dec;28(24):e70313. doi: 10.1111/jcmm.70313.

DOI:10.1111/jcmm.70313
PMID:39730981
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11680193/
Abstract

Despite improvements in interventional techniques leading to faster myocardial reperfusion postmyocardial infarction, there has been a significant rise in the occurrence of myocardial ischaemia/reperfusion injury (MI/RI). A deeper understanding of the underlying mechanisms of MI/RI could offer a crucial approach to reducing myocardial damage and enhancing patient outcomes. This study examined the myocardial protective properties of puerarin (PUE) in the context of MI/RI using hypoxia/reoxygenation (H/R) or ischaemia/reperfusion (I/R) injury models were employed in H9c2 cells and C57BL/6 mice. Our findings demonstrate that pretreatment with PUE effectively mitigated cardiomyocyte ferroptosis, restored redox balance, preserved mitochondrial energy production and maintained mitochondrial function following MI/RI. Furthermore, these cardioprotective effects of PUE were found to be mediated by the downregulation of voltage-dependent anion channel 1 (VDAC1) protein. These data reveal a novel mechanism by which PUE inhibits MI/RI and reveal that this protective effect of PUE is dependent on the downregulation of VDAC1.

摘要

尽管介入技术有所改进，使心肌梗死后心肌再灌注更快，但心肌缺血/再灌注损伤（MI/RI）的发生率仍显著上升。深入了解MI/RI的潜在机制可能为减少心肌损伤和改善患者预后提供关键方法。本研究在H9c2细胞和C57BL/6小鼠中使用缺氧/复氧（H/R）或缺血/再灌注（I/R）损伤模型，研究了葛根素（PUE）在MI/RI情况下的心肌保护特性。我们的研究结果表明，PUE预处理可有效减轻心肌细胞铁死亡，恢复氧化还原平衡，在MI/RI后维持线粒体能量产生并保持线粒体功能。此外，发现PUE的这些心脏保护作用是由电压依赖性阴离子通道1（VDAC1）蛋白的下调介导的。这些数据揭示了PUE抑制MI/RI的新机制，并表明PUE的这种保护作用依赖于VDAC1的下调。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/4f572e3b2955/JCMM-28-e70313-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/145c14befba8/JCMM-28-e70313-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/24d052d9dd23/JCMM-28-e70313-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/6c2bd3bf7a15/JCMM-28-e70313-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/8cc044e9e4b4/JCMM-28-e70313-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/adbccae789d3/JCMM-28-e70313-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/f044b91d1afe/JCMM-28-e70313-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/838b10c0d68a/JCMM-28-e70313-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/4f572e3b2955/JCMM-28-e70313-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/145c14befba8/JCMM-28-e70313-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/24d052d9dd23/JCMM-28-e70313-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/6c2bd3bf7a15/JCMM-28-e70313-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/8cc044e9e4b4/JCMM-28-e70313-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/adbccae789d3/JCMM-28-e70313-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/f044b91d1afe/JCMM-28-e70313-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/838b10c0d68a/JCMM-28-e70313-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec66/11680193/4f572e3b2955/JCMM-28-e70313-g004.jpg

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