Anti-endometriosis Mechanism of Jiawei Foshou San Based on Network Pharmacology

Abstract

<i>Jiawei Foshou San</i> (JFS) is the new formula originated from classic <i>Foshou San</i> formula, composed with ligustrazine, ferulic acid, and tetrahydropalmatine. Previously JFS inhibited the growth of endometriosis (EMS) with unclear mechanism, especially in metastasis, invasion, and epithelial-mesenchymal transition. In this study, network pharmacology was performed to explore potential mechanism of JFS on EMS. Through compound-compound target and compound target-EMS target networks, key targets were analyzed for pathway enrichment. MMP-TIMP were uncovered as one cluster of the core targets. Furthermore, autologous transplantation of EMS rat's model were used to evaluate <i>in vivo</i> effect of JFS on invasion, metastasis and epithelial-mesenchymal transition. JFS significantly suppressed the growth, and reduced the volume of ectopic endometrium, with modification of pathologic structure. In-depth study, invasion and metastasis were restrained after treating with JFS through decreasing MMP-2 and MMP-9, increasing TIMP-1. Meanwhile, JFS promoted E-cadherin, and attenuated N-cadherin, Vimentin, Snail, Slug, ZEB1, ZEB2, Twist. In brief, anti-EMS effect of JFS might be related to the regulation of epithelial-mesenchymal transformation, thereby inhibition of invasion and metastasis. These findings reveal the potential mechanism of JFS on EMS and the benefit for further evaluation.