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

机译:基于网络药理学的加味佛手散抗子宫内膜异位症机制

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摘要

Jiawei Foshou San (JFS) is the new formula originated from classic Foshou San 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 in vivo 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.
机译:加味佛手散(JFS)是源自经典佛手散配方的新配方,由川azine嗪,阿魏酸和四氢巴马汀组成。以前,JFS抑制子宫内膜异位症(EMS)的生长机理尚不清楚,尤其是在转移,侵袭和上皮间质转化中。在这项研究中,进行网络药理学以探讨JFS在EMS上的潜在机制。通过复合目标和复合目标EMS目标网络,分析了关键目标的途径富集。 MMP–TIMP被发现为核心目标的一个集群。此外,EMS大鼠模型的自体移植被用于评估JFS对侵袭,转移和上皮-间质转化的体内作用。 JFS明显抑制了其生长,并减少了异位子宫内膜的体积,并改变了病理结构。深入研究发现,JFS治疗后通过减少MMP-2和MMP-9,增加TIMP-1来抑制其侵袭和转移。同时,JFS促进了E-钙黏着蛋白,并减弱了N-钙黏着蛋白,波形蛋白,蜗牛,Slug,ZEB1,ZEB2,Twist。简而言之,JFS的抗EMS作用可能与上皮-间质转化的调控有关,从而抑制其侵袭和转移。这些发现揭示了JFS在EMS上的潜在机制以及进一步评估的好处。

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