[Study on mechanism of Rhei Radix et Rhizoma-Persicae Semen in treatment of adenomyosis based on network pharmacology].

The aim of this paper was to screen the active targets of Rhei Radix et Rhizoma and Persicae Semen in the treatment of adenomyosis(AM) by means of network pharmacology, and to investigate their mechanism of action. The effective components of Rhei Radix et Rhizoma and Persicae Semen were screened out by using traditional Chinese medicine systematic pharmacological(TCMSP) database, with oral bioavilability(OB) ≥30% and drug-like(DL) ≥0.18 selected as the thresholds. A network was built between the main components and their corresponding targets. Ninety-five human genes corresponding to the medicine targets were obtained from Uniprot database; 220 genes corresponding to AM were obtained from GeneCards database. A total of 21 intersection genes were screened from disease genes and medicine genes, and the protein-protein interaction network interaction(PPI)analysis was conducted by using STRING tool. Disease-target PPI network was drawn by using Cytoscape software, and component-target-disease network was constructed. Twenty-five nodes and 74 connections were found, and then core networks and targets were screened for Kyoto encyclopedia of genes and genomes(KEGG) pathway enrichment analysis. The animal model of AM was established by feeding tamoxifen citrate mixed droplets to primary mice for verification of the mechanism. Twenty-three signaling pathways were involved in KEGG pathway enrichment. It was found that the therapeutic mechanism of Rhei Radix et Rhizoma and Persicae Semen on AM may involve multiple targets such as inflammation and immunity, proliferation and apoptosis, endocrine and oxidative stress. Among them, the P53 signaling pathway and the apoptotic signaling pathway which mediated the expression of P53 and BAX may be the important ones. Animal experiments proved that the effective components of Rhei Radix et Rhizoma and Persicae Semen can interfere with the P53 signaling pathway and the apoptotic signaling pathway at the junction of endometrial muscle layer, increase the expression of P53 and BAX in muscle layer cells, and promote the apoptosis of cells with abnormal proliferation ability.