Mediators of inflammation · 2026
Tubal Patency Decoction and Its Ingredient β-Sitosterol Alleviate Tubal Infertility by Inhibiting Inflammation and Promoting Cilia Formation Through PGR.
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Shao Liang, Wang Nansu, Yan Yan, Tan Qiongfang, Huang Yuying, Wu Qin, Tan Yali, Zhu Yue, Xia Yaqiong, Liu Ling
Аннотация
BACKGROUND: Tubal infertility is one of the major causes of female infertility. This study aimed to investigate the mechanism of action of tubal patency decoction (TPD) and its active ingredient β-sitosterol on tubal infertility.
METHODS: The active ingredients of TPD and their potential targets were obtained from the TCMSP and Batman-TCM databases. The GeneCards, NCBI, and OMIM databases provided the targets associated with tubal infertility. The relationship between the components of TPD and the potential targets of tubal infertility was analyzed by String database and Cytoscape 3.8.0 software. The composition of the compounds in TPD was examined by liquid chromatography-mass spectrometry (LC-MS) assay. The effects of TPD and β-sitosterol on tubal infertility were verified by establishing a rat model of tubal infertility and a model of tubal epithelial cell inflammation.
RESULTS: By network pharmacological analysis, we screened 139 active ingredients of TPD, covering 523 targets, of which 34 were related to tubal infertility. β-sitosterol was identified as an important active compound. Progesterone receptor (PGR) was considered the main target of TPD and β-sitosterol in tubal infertility. Molecular docking and drug affinity responsive target stability (DARTS) assays showed that PGR binds to β-sitosterol. The results of cellular experiments confirmed that β-sitosterol and TPD-containing serum increased the cell viability of LPS-induced tubal epithelial cells, decreased the levels of inflammatory factors (IL-1β, IL-6, IL-8, and TNF-α) and myeloperoxidase (MPO), and increased the frequency of ciliary beating. The results of in vivo experiments showed that both TPD and β-sitosterol improved the conception rate and live births in tubal infertile rats and attenuated tubal inflammation and epithelial cell damage. They increased the expression of RFX2, RFX3, and FOXJ1. Silencing PGR reversed the effect of β-sitosterol on tubal epithelial cells and tubal infertile rats.
CONCLUSION: TPD and its active ingredient β-sitosterol may improve tubal infertility through PGR. These results provide a new basis for the development and application of TPD and its active ingredient β-sitosterol.
METHODS: The active ingredients of TPD and their potential targets were obtained from the TCMSP and Batman-TCM databases. The GeneCards, NCBI, and OMIM databases provided the targets associated with tubal infertility. The relationship between the components of TPD and the potential targets of tubal infertility was analyzed by String database and Cytoscape 3.8.0 software. The composition of the compounds in TPD was examined by liquid chromatography-mass spectrometry (LC-MS) assay. The effects of TPD and β-sitosterol on tubal infertility were verified by establishing a rat model of tubal infertility and a model of tubal epithelial cell inflammation.
RESULTS: By network pharmacological analysis, we screened 139 active ingredients of TPD, covering 523 targets, of which 34 were related to tubal infertility. β-sitosterol was identified as an important active compound. Progesterone receptor (PGR) was considered the main target of TPD and β-sitosterol in tubal infertility. Molecular docking and drug affinity responsive target stability (DARTS) assays showed that PGR binds to β-sitosterol. The results of cellular experiments confirmed that β-sitosterol and TPD-containing serum increased the cell viability of LPS-induced tubal epithelial cells, decreased the levels of inflammatory factors (IL-1β, IL-6, IL-8, and TNF-α) and myeloperoxidase (MPO), and increased the frequency of ciliary beating. The results of in vivo experiments showed that both TPD and β-sitosterol improved the conception rate and live births in tubal infertile rats and attenuated tubal inflammation and epithelial cell damage. They increased the expression of RFX2, RFX3, and FOXJ1. Silencing PGR reversed the effect of β-sitosterol on tubal epithelial cells and tubal infertile rats.
CONCLUSION: TPD and its active ingredient β-sitosterol may improve tubal infertility through PGR. These results provide a new basis for the development and application of TPD and its active ingredient β-sitosterol.