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

• Published in: Journal of cellular and molecular medicine 2024-11, Vol.28 (22), p.e70236-n/a
• Main Authors: Zuo, Yue, Wang, Jiawei, Gong, Zhexuan, Wang, Yulong, Wang, Qiang, Yang, Xueyang, Liu, Fulin, Liu, Tongtong
• Format: Article
• Language: English
• Subjects: Angioplasty; Animals; Apoptosis; Apoptosis - drug effects; BAX protein; Bcl-2 protein; Biosynthesis; Caspase; Coronary vessels; H9C2rat myocardial cells; Heart attacks; Heart failure; Heart surgery; Homeostasis; Hydrogen; Hydrogen - pharmacology; Hypoxia; Inflammation; Ischemia; Laboratory animals; Male; Metabolism; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Mitochondria, Heart - drug effects; Mitochondria, Heart - metabolism; Mitochondria, Heart - ultrastructure; Mitochondrial DNA; Mitochondrial Dynamics - drug effects; myocardial ischaemia–reperfusion injury; Myocardial Reperfusion Injury - drug therapy; Myocardial Reperfusion Injury - genetics; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - pathology; Myocardium - metabolism; Myocardium - pathology; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; Myocytes, Cardiac - pathology; Original; Ostomy; Permeability; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - metabolism; PGC‐1α; Phosphorylation; Physiology; Rats; Rats, Sprague-Dawley; Reperfusion; Transmission electron microscopy; Veins & arteries
• ISSN: 1582-1838; 1582-4934; 1582-4934
• DOI: 10.1111/jcmm.70236

ABSTRACT To investigate the application of H2 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, Bcl2), 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 H2 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 H2 treatment. H2 increases the expression level of PGC‐1α, while the deletion of PGC‐1α inhibited the therapeutic effect of H2. H2 can improve the changes of the myocardial tissue and mitochondrial structure caused by I/R injury. H2 treatment effectively inhibited the inflammatory response, and the loss of PGC‐1α could inhibit the therapeutic effect of H2. The application of H2 can alleviate myocardial I/R injury, and the loss of PGC‐1α weakens the protective effect of H2 on the I/R heart.