{"paper_id":"4528ef35-6bf6-4917-ba54-a7bf1d8f0868","body_text":"Bushen Xiaozheng Decoction Improves Immunosuppression in a Rat Model of Endometriosis by Reducing IL-10 and TGF-β Levels\nABSTRACT\nProblem\nHow does the traditional Chinese compound Bushen Xiaozheng Decoction (BSXZD) affect the immunosuppressive microenvironment in rat endometriosis models?\nMethods\nSprague Dawley rats were randomly divided into normal, sham operation, model, Yasmin, and low-, medium-, high-dose BSXZD groups with 10 rats in each group. The endometriosis model was established by autologous endometrial transplantation, and corresponding interventions were given for 28 days. The volume of ectopic lesions was measured, and histological changes of endometrium were observed by hematoxylin-eosin staining. The protein or gene expression of interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) in serum or endometrium was detected by immunohistochemistry, quantitative real-time polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay.\nResults\nFollowing treatment with BSXZD, the pseudostratified phenomenon and cavity structure of endometrial cells were reduced. Additionally, the expression levels of IL-10 and TGF-β in both endometrium and serum were significantly decreased, accompanied by a marked reduction in the volume of ectopic lesions.\nConclusion\nBSXZD can significantly inhibit the growth of ectopic lesions in a rat model of endometriosis. The underlying mechanism may involve dual regulation of the endocrine-immune axis: it not only directly downregulates the expression of the immunosuppressive factors IL-10 and TGF-β to reversing the local immunosuppressive microenvironment, but also indirectly modulates these cytokines via sex hormone-related signaling pathways. Further studies are needed to clarify the precise molecular mechanism.\nConflicts of Interest\nThe authors declare no conflict of interest.\nData Availability Statement\nThe data that support the findings of this study are available from the corresponding author upon reasonable request.","source_license":"public-domain-us","license_restricted":false}