Tissue & cell · 2025
Hypericin attenuates myocardial ischemia-reperfusion injury by enhancing mitochondrial energy metabolism via AMPK/PGC-1α signaling pathway.
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Huihui L I, Yali Bao, Wanyue L I, Huitian Xin, Xiaofeng Gao, Ainiwar Dina, Can Ling, Anwaier Gulinigaer, Zhan Sun
Аннотация
BACKGROUND: Although blood flow is restored following the treatment of acute myocardial infarction (AMI), myocardial Ischaemia /reperfusion can still cause cardiac damage, potentially leading to cardiac decompensation and, ultimately, heart failure. This study aimed to investigate the effects of Hypericin (Hyp) on the hearts of rats with myocardial ischaemia-reperfusion injury (MIRI) and its underlying mechanisms.
METHODS: Male Sprague-Dawley rats and H9C2 cells underwent MIRI and hypoxia/reoxygenation (H/R) modelling after Hyp administration to assess the compound's effects on cardiac and cardiomyocyte characteristics, as well as mitochondrial energy metabolism. A range of techniques, including 2,3,5-triphenyltetrazolium chloride staining, haematoxylin-eosin staining, echocardiography, enzyme-linked immunosorbent assay, quantitative proteomics analysis, molecular docking, and Western blotting were employed to further characterize Hyp's cardioprotective effects and its influence on related molecular expressions. TUNEL staining and Western blotting were also used to examine the morphological, molecular, and functional phenotypes of H/R-treated cardiomyocytes.
RESULTS: Hyp significantly reduced myocardial infarct size and improved cardiac function in MIRI rats. Hyp increased cardiomyocyte viability while decreasing cardiomyocyte damage. The cardioprotective effects of Hyp were primarily mediated by alleviating mitochondrial dysfunction and oxidative stress, mainly through the adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1-alpha (PGC-1α) signalling pathway.
CONCLUSION: Hyp regulates the AMPK/PGC-1α signalling pathway to improve mitochondrial energy metabolism and reduce oxidative stress, thereby mitigating MIRI in rats.
METHODS: Male Sprague-Dawley rats and H9C2 cells underwent MIRI and hypoxia/reoxygenation (H/R) modelling after Hyp administration to assess the compound's effects on cardiac and cardiomyocyte characteristics, as well as mitochondrial energy metabolism. A range of techniques, including 2,3,5-triphenyltetrazolium chloride staining, haematoxylin-eosin staining, echocardiography, enzyme-linked immunosorbent assay, quantitative proteomics analysis, molecular docking, and Western blotting were employed to further characterize Hyp's cardioprotective effects and its influence on related molecular expressions. TUNEL staining and Western blotting were also used to examine the morphological, molecular, and functional phenotypes of H/R-treated cardiomyocytes.
RESULTS: Hyp significantly reduced myocardial infarct size and improved cardiac function in MIRI rats. Hyp increased cardiomyocyte viability while decreasing cardiomyocyte damage. The cardioprotective effects of Hyp were primarily mediated by alleviating mitochondrial dysfunction and oxidative stress, mainly through the adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor γ coactivator 1-alpha (PGC-1α) signalling pathway.
CONCLUSION: Hyp regulates the AMPK/PGC-1α signalling pathway to improve mitochondrial energy metabolism and reduce oxidative stress, thereby mitigating MIRI in rats.