Exploring the Cardioprotective Mechanisms of in Myocardial Infarction Through Network Pharmacology and Experimental Validation.

BACKGROUND

Myocardial infarction represents a coronary artery ailment with the highest incidence and fatality rates among cardiovascular conditions. However, effective pharmacological interventions remain elusive. This study seeks to elucidate the molecular mechanisms underlying the effects of on myocardial infarction through network pharmacology and experimental validation.

METHODS

Initially, potential targets of 's active ingredients and myocardial infarction-related targets were retrieved from databases. Subsequently, core targets of on myocardial infarction were identified via the PPI network analysis and subjected to GO and KEGG pathway enrichment analyses. Molecular docking was employed to validate the binding affinities between the core targets and the bioactive components. The findings from network pharmacology analysis were corroborated through in vitro in vivo experiments.

RESULTS

Seven active ingredients from were identified, corresponding to 122 targets. Molecular docking revealed robust binding affinities of Myricanone, Senkyunone, and Sitosterol to key target proteins (EGFR, STAT3, and SRC). In vitro, experiments demonstrated that pretreatment with the active components of protected myocardial cells from OGD exposure and modulated the expression of their key target genes. In vivo, experiments showed that the active components of significantly improved myocardial infarction via alleviating myocardial fibrosis and oxidative stress and did not elicit toxic effects in mice.

CONCLUSION

The collective findings suggest that shows promising potential for myocardial infarction treatment by regulating key target proteins (EGFR, STAT3, and SRC), which play roles in oxidative stress and myocardial fibrosis.