Moxibustion at Guanyuan (CV4) Inhibits Endometriosis Progression via Regulation of the Wnt/β-catenin Signalling Pathway in a Murine Model

Objective: To observe the effects of moxibustion on the regulation of the Wnt/β-catenin signal-ling pathway, inhibition of cyst growth, and the expressions of uPA, MMP 9, E-cadherin, Axin, GSK3β, and β-catenin in a mouse model of endometriosis (EMs). The study aimed to explore the mechanism by which moxibustion regulates Wnt/β-catenin signalling to inhibit endometrial adhesion and reconstruction.Methods: A total of 42 female BALB/c mice, aged 8 weeks, were divided into a control group (Group A) with 8 mice and an experimental group of 34 mice using random distribution. In the experimental group, EMs mouse model was induced by the auto-transplantation method and was further sub-divided into EMs model group (Group B), Cake-separated moxibustion at the Guanyuan acupoint (CV4) group (Group C), Agonist group (Group D) and Inhibitor group (Group E), having 8 mice per each sub-group. After successful modelling, the experimental groups underwent respective interventions for 14 consecutive days. Following treatment, the size of the cysts was observed, and the expression of key proteins such as uPA, MMP 9, E-cadherin, Axin, GSK3β, and β-catenin in ectopic endometrial tissues was assessed using west-ern blot.Results: Relatively to the control group all parameters were considered normal. Comparatively to model Group B and the agonist Group D, the present results in moxibustion Group C and the inhibitor Group E show that: the number of writhing reactions was significantly reduced (both P < 0.05); the overall volume of ectopic cysts significantly decreased (both P < 0.05); the protein grayscale values of Axin, GSK3β, and β-catenin were significantly lower (all P < 0.05); the protein grayscale values of uPA and MMP 9 were significantly lower (all P < 0.05); the E-cadherin was significantly higher too (all P < 0.05).Conclusion: Moxibustion at the CV4 acupoint can alleviate dysmenorrhea symptoms, inhibit the growth of endometriosis cysts, regulate the Wnt/β-catenin signalling pathway, suppress the ac-tivation of the Wnt/β-catenin signalling pathway, reduce the expression of downstream factors uPA and MMP 9, inhibit the adhesion and reconstruction of ectopic endometrial cells, promote the expression of E-cadherin, enhance the adhesion between normal endometrial cells, prevent the adhesion and cell migration process, and prevent the reconstruction of the matrix and base-ment membrane.