β-Sitosterol Inhibits The Proliferation of Endometrial Cells via Regulating Smad7-Mediated TGF-β/Smads Signaling Pathway.

Yi Wen, Lili Pang, Lingxiu Fan, Ling-Xiu Fan, Yihan Zhou, Ruonan Li, Tingting Zhao, Manli Zhang
Cell journal · 2023 · vol. 25(8) , pp. 554–563 · doi:10.22074/cellj.2023.1989631.1230 · PMID:37641417 · PMC10542208 · W4386271506
article OA: gold CC0 ⤵ 2 in-corpus citations
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Abstract

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.

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endometriosis

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