Document Type : Original Article
Departments of Gynecology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan, China
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.