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

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.