Ontology highlight
ABSTRACT: Cardiovascular adverse effects caused by high-intensity exercise (HIE) have become a public health problem of widespread concern. As a phytochemical with potential therapeutic effects, the therapeutic effect and metabolic regulation mechanism of myricetin have rarely been studied. In this study, we established different doses of myricetin intervention with 1 week of HIE after intervention. Cardiac function tests, serology and pathological examinations were used to evaluate the protective effect of myricetin on the myocardium. The possible therapeutic targets of myricetin were obtained using integrated analysis of metabolomics and network pharmacology and verified using molecular docking and RT-qPCR experiments. Different concentrations of myricetin improved cardiac function, significantly reduced the levels of myocardial injury markers, alleviated myocardial ultrastructural damage, reduced the area of ischemia/hypoxia, and increased the content of CX43. Through combined analysis with metabolomics and network pharmacology and then verification with molecular docking and RT-qPCR, we found that PTGS2, MAOB, EGFR, MAP2K1 were the key targets for injury protection. Arachidonic acid metabolism, glycine-serine-threonine acid metabolism and FoxO metabolism may be the key metabolic pathways affected by myricetin intervention. In summary, our findings suggest that myricetin exert cardiac protective effects of HIE by regulating myocardial metabolic network.
INSTRUMENT(S): Liquid Chromatography MS - positive - hilic, Liquid Chromatography MS - negative - hilic
SUBMITTER: Tianyou Li
PROVIDER: MTBLS5608 | MetaboLights | 2023-03-06
REPOSITORIES: MetaboLights
Action | DRS | |||
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MTBLS5608 | Other | |||
FILES | Other | |||
a_MTBLS5608_LC-MS_negative_hilic_metabolite_profiling.txt | Txt | |||
a_MTBLS5608_LC-MS_positive_hilic_metabolite_profiling.txt | Txt | |||
files-all.json | Other |
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