β-sitosterol inhibits the proliferation of endometrial cells via regulating smad7-mediated tgf-β/smads signaling pathway

Objective: to investigate the effect of β-sitosterol on endometrial cells to understand the underlying mechanism. materials and methods: this is a laboratory-based experimental study conducted on animals and cells. histological assays were performed to determine the effect of β-sitosterol on endometrial cells. the cck-8 assay was used to assess the inhibitory effect of β-sitosterol on the proliferation of ectopic endometrial stromal cells (hem15a). flow cytometry was performed to evaluate the induction of apoptosis by β-sitosterol in hem15a cells. the transwell invasion assay was conducted to measure the suppression of hem15a cell migration by β-sitosterol. western blot analyses were performed to analyze the effect of β-sitosterol on the expression of smad family member 7 (smad7) and the activity of transforming growth factor-β (tgf-β1), as well as the phosphorylation of smad2 and smad3. results: histological assays showed that β-sitosterol regulates histopathology and induces apoptosis of endometrial cells in vivo. the cck-8 assay revealed that β-sitosterol could inhibit the proliferation of hem15a in human endometriosis patients. flow cytometry showed that apoptosis was triggered by β-sitosterol in hem15a. the transwell invasion assay indicated that the hem15a migration under the β-sitosterol treatment group was suppressed. western blot analyses suggested that β-sitosterol increased the expression of smad7, decreased the activity of tgf-β1, and reduced the phosphorylation of smad2 and smad3. the effect of β-sitosterol was weakened by the silence of smad7. conclusion: the results suggest that β-sitosterol can inhibit the proliferation of endometrial cells and relieve endometriosis by inhibiting tgf-β-induced phosphorylation of smads through regulation of smad7.