Abstract
The aim of this study was to investigate the precise effects and mechanisms of bergamottin in heart failure. Oxygen-glucose deprivation and reperfusion was used to simulate H9C2 cell injury in heart failure. Cell Counting Kit-8 and lactate dehydrogenase kits were used to assess cell viability. JC-1 stain, reactive oxygen species, and adenosine triphosphate kits were utilized to probe mitochondrial status. In addition, oxidative stress indicators were analyzed by enzyme-linked immunosorbent assay. Bergamottin treatment reduced lactate dehydrogenase and enhanced cell survival. Furthermore, oxygen-glucose deprivation and reperfusion-induced mitochondrial function was recovered, and oxidative stress levels were decreased by bergamottin therapy. Finally, mechanistic research showed that the SIRT1/AMPK pathway was activated by bergamottin. Bergamottin could be a potential drug for the clinical treatment of heart disease.
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