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氢气通过增加 PGC-1α 的表达和改善心肌缺血再灌注损伤来保护线粒体功能。

Hydrogen Protects Mitochondrial Function by Increasing the Expression of PGC-1α and Ameliorating Myocardial Ischaemia-Reperfusion Injury.

机构信息

Heart Center, The First Hospital of Tsinghua University, Beijing, China.

School of Clinical Medicine, Hebei University, Baoding, China.

出版信息

J Cell Mol Med. 2024 Nov;28(22):e70236. doi: 10.1111/jcmm.70236.

DOI:10.1111/jcmm.70236
PMID:39601332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11600203/
Abstract

To investigate the application of H to alleviate cardiac ischaemia-reperfusion (I/R) injury in a PGC-1α-dependent manner. A rat in vitro myocardial I/R injury model was used, Western blot was used to detect the expression levels of apoptosis markers (Bax, cleaved caspase-3, Bcl), inflammatory factors (IL-1β, TNF-α), mitochondrial fission (DRP1, MFF) and mitochondrial fusion (MFN1, MFN2, OPA1). HE staining was used to observe the effect of H on the myocardial tissue structure injured by I/R. Transmission electron microscopy (TEM) was used to observe the changes in the mitochondrial structure of myocardial tissue after I/R injury. Real-time quantitative PCR (qPCR) was used to detect the expression of PGC-1α in the myocardial tissue of rats after I/R injury and H treatment. H increases the expression level of PGC-1α, while the deletion of PGC-1α inhibited the therapeutic effect of H. H can improve the changes of the myocardial tissue and mitochondrial structure caused by I/R injury. H treatment effectively inhibited the inflammatory response, and the loss of PGC-1α could inhibit the therapeutic effect of H. The application of H can alleviate myocardial I/R injury, and the loss of PGC-1α weakens the protective effect of H on the I/R heart.

摘要

为了研究 H 通过依赖 PGC-1α 减轻心肌缺血再灌注(I/R)损伤的应用。建立了大鼠体外心肌 I/R 损伤模型,用 Western blot 检测凋亡标志物(Bax、cleaved caspase-3、Bcl)、炎症因子(IL-1β、TNF-α)、线粒体分裂(DRP1、MFF)和线粒体融合(MFN1、MFN2、OPA1)的表达水平。HE 染色观察 H 对 I/R 损伤心肌组织结构的影响。透射电镜(TEM)观察 I/R 损伤后心肌组织中线粒体结构的变化。实时定量 PCR(qPCR)检测 I/R 损伤和 H 处理后大鼠心肌组织中 PGC-1α 的表达。H 增加了 PGC-1α 的表达水平,而 PGC-1α 的缺失抑制了 H 的治疗作用。H 可改善 I/R 损伤引起的心肌组织和线粒体结构的变化。H 处理有效抑制了炎症反应,而 PGC-1α 的缺失抑制了 H 的治疗作用。H 的应用可以减轻心肌 I/R 损伤,而 PGC-1α 的缺失会削弱 H 对 I/R 心脏的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/af9af18c985f/JCMM-28-e70236-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/c0cf7e938c64/JCMM-28-e70236-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/4cb355ef833e/JCMM-28-e70236-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/36d28289c2e0/JCMM-28-e70236-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/af9af18c985f/JCMM-28-e70236-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/c0cf7e938c64/JCMM-28-e70236-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/4cb355ef833e/JCMM-28-e70236-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/36d28289c2e0/JCMM-28-e70236-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad1a/11600203/af9af18c985f/JCMM-28-e70236-g002.jpg

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