Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026
Shaofu Zhuyu decoction can inhibit the progression of endometriosis fibrosis through the transforming growth factor-β1/ smads signaling pathway mediated by 5' adenosine monophosphate-activated protein kinase.
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Bingbing L I, Meiqi Ding, Xiangying Chen, Wenzhe L I, Chao Wei, Bin Y U, Xiaona M A, Xinhui Sun
Аннотация
OBJECTIVE: To investigate the mechanisms by which Shaofu Zhuyu decoction (SFZYD, ) modulates fibrosis in a mouse model of endometriosis.
METHODS: Mice were divided into control, endometriosis model, low-dose SFZYD, high-dose SFZYD, and dinorgestrel groups. Ectopic lesion weights and volumes were evaluated post-intervention. Uterine or lesion morphology and fibrosis were assessed using hematoxylin/eosin and Masson's trichrome and Sirius red staining, respectively. Gene expression levels of 5' adenosine monophosphate-activated protein kinase (AMPK), transforming growth factor β1 (TGF-β1), collagen type 1 alpha 1 chain (COL1A1), alpha smooth muscle actin (α-SMA), and connective tissue growth factor (CTGF) were detected using quantitative real-time polymerase chain reaction. Protein expression levels of AMPK, p-AMPK, TGF-β1, Smad2/3, p-Smad2/3, COL1A1, α-SMA and CTGF were detected using immunohistochemistry or Western blotting.
RESULTS: Staining revealed excessive ectopic lesion fibrosis, and p-AMPK/AMPK expression was downregulated in the model group, whereas TGF-β1, Smad2/3, COL1A1, α-SMA, and CTGF expression was upregulated. SFZYD-L group showed the greatest effect in reducing ectopic lesion size and inhibiting fibrosis. These changes were correlated with the activation/ phosphorylation of AMPK, suppression of TGF-β1 and Smad2/3 expression, and downregulation of COL1A1, α-SMA, and CTGF expression, suggesting a potential association with AMPK modulation.
CONCLUSION: SFZYD significantly inhibits both the progression of ectopic lesions and the development of fibrosis in a mouse model of endometriosis. These effects are potentially mediated through the regulation of the AMPK/TGF-β1/Smads signaling pathway.
METHODS: Mice were divided into control, endometriosis model, low-dose SFZYD, high-dose SFZYD, and dinorgestrel groups. Ectopic lesion weights and volumes were evaluated post-intervention. Uterine or lesion morphology and fibrosis were assessed using hematoxylin/eosin and Masson's trichrome and Sirius red staining, respectively. Gene expression levels of 5' adenosine monophosphate-activated protein kinase (AMPK), transforming growth factor β1 (TGF-β1), collagen type 1 alpha 1 chain (COL1A1), alpha smooth muscle actin (α-SMA), and connective tissue growth factor (CTGF) were detected using quantitative real-time polymerase chain reaction. Protein expression levels of AMPK, p-AMPK, TGF-β1, Smad2/3, p-Smad2/3, COL1A1, α-SMA and CTGF were detected using immunohistochemistry or Western blotting.
RESULTS: Staining revealed excessive ectopic lesion fibrosis, and p-AMPK/AMPK expression was downregulated in the model group, whereas TGF-β1, Smad2/3, COL1A1, α-SMA, and CTGF expression was upregulated. SFZYD-L group showed the greatest effect in reducing ectopic lesion size and inhibiting fibrosis. These changes were correlated with the activation/ phosphorylation of AMPK, suppression of TGF-β1 and Smad2/3 expression, and downregulation of COL1A1, α-SMA, and CTGF expression, suggesting a potential association with AMPK modulation.
CONCLUSION: SFZYD significantly inhibits both the progression of ectopic lesions and the development of fibrosis in a mouse model of endometriosis. These effects are potentially mediated through the regulation of the AMPK/TGF-β1/Smads signaling pathway.