Effect and Mechanism of Fisetin on Patulin Induced Myocardial Damage Based on Network Pharmacology

Abstract

Abstract Objectives of the Study The aim of this study is to investigate whether fisetin can effectively reduce patulin induced myocardial damage, and to reveal the mechanism and target of fisetin in inhibiting myocardial damage. Materials and Methods: Network pharmacology was used to screen the targets of fisetin on myocardial damage, the regulatory network of active ingredients-drug targets was constructed, and GO and KEGG enrichment analysis were performed to screen out the key pathways and targets of fisetin on myocardial damage. Patulin was used to induce apoptosis in H9c2 cardiomyocytes to verify the key targets. The mechanism of fisetin inhibiting myocardial damage was determined. Results FIS can reduce the apoptosis of cardiomyocytes by protecting cardiomyocytes from PAT injury. According to the results of network pharmacology analysis, combined with enzyme activity detection and WB experiment, it was found that the mechanism of FIS to reduce myocardial damage may be related to P53 signaling pathway, Caspase3/8/9 and Bax/Bcl-2. Conclusion FIS plays a protective role in PAT-induced myocardial damage by inhibiting the protein overexpression of P53, Caspase-9 and Bax and enhancing the protein expression of Bcl-2.