Inhibition of the Jagged-1/Notch1/Hes1 Signaling Pathway by Evodiamine Attenuates Epithelial-Mesenchymal Transition in Mice with Adenomyosis

Xiaorui Dong, Xixi Chen, Mengling Xue, Yina Zhang
In: JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS · 2023 · vol. 37(8) · doi:10.23812/j.biol.regul.homeost.agents.20233708.420 · W4407292373
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Evodiamine attenuates epithelial-mesenchymal transition and reduces endometrial infiltration in adenomyosis by inhibiting the Jagged-1/Notch1/Hes1 signaling pathway, as demonstrated in human tissues and a mouse model.

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This study investigated the therapeutic potential of evodiamine in mitigating adenomyosis by targeting the Jagged-1/Notch1/Hes1 signaling pathway. Researchers analyzed endometrial tissues from human patients and utilized a tamoxifen-induced mouse model to evaluate the effects of evodiamine on epithelial-mesenchymal transition markers such as E-cadherin, N-cadherin, and alpha-smooth muscle actin. The findings demonstrated that evodiamine inhibited this specific signaling pathway, thereby reducing endometrial infiltration into the myometrium and decreasing collagen deposition in both human samples and animal models. This paper is centrally about adenomyosis — specifically, it proposes evodiamine as a treatment option that attenuates disease progression by suppressing epithelial-mesenchymal transition via the Jagged-1/Notch1/Hes1 axis.

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Abstract

Background: Evodiamine has been documented to suppress epithelial-mesenchymal transition (EMT), but its effects on adenomyosis are poorly understood. This study investigates evodiamines potential effects and mechanisms in treating adenomyosis. Methods: The cohort comprised 90 women (34 healthy controls and 56 adenomyosis patients). The Jagged-1/Notch1/hairy expression levels and hairy and enhancer of split 1 (Hes1) signaling pathway in human endometrial tissues were assessed using western blot analysis. An adenomyosis mouse model was created using 1 mg/kg tamoxifen, followed by treatment with evodiamine and dual antiplatelet therapy (DAPT). Expression levels of alpha-smooth muscle actin (α-SMA), collagen I, neural cadherin (N-cadherin), epithelial cadherin (E-cadherin), Snail, and Vimentin were evaluated using western blot analysis. Immunohistochemistry was used to assess Jagged-1, Notch1, and Hes1 levels. Hematoxylin and eosin (H&E) staining evaluated the depth of endometrial infiltration into the myometrium, and Masson trichrome staining quantified collagen content. Results: The Jagged-1/Notch1/(hairy and enhancer of split 1) Hes1 pathway was found to be activated in the endometrial tissues of adenomyosis patients. In adenomyosis mice, evodiamine treatment led to the inhibition of the Jagged-1/Notch1/Hes1 pathway, along with observable morphological changes, such as reduced adenomyosis nodules with congestion. This improvement was significant compared to the control group ( p < 0.05). Furthermore, evodiamine and DAPT treatments reduced endometrial infiltration into the myometrium and collagen deposition while suppressing the expression of α-SMA, collagen I, N-cadherin, Snail, and Vimentin, and upregulating E-cadherin expression. The inhibitory effect was significantly greater than that in the control group ( p < 0.05). Conclusion: Evodiamine mitigated adenomyosis by regulating EMT through the inactivation of the Jagged-1/Notch1/Hes1 pathway. This finding suggests that evodiamine could be a potential treatment option for adenomyosis.
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Abstract

Background: Evodiamine has been documented to suppress epithelial-mesenchymal transition (EMT), but its effects on adenomyosis are poorly understood. This study investigates evodiamines potential effects and mechanisms in treating adenomyosis. Methods: The cohort comprised 90 women (34 healthy controls and 56 adenomyosis patients). The Jagged-1/Notch1/hairy expression levels and hairy and enhancer of split 1 (Hes1) signaling pathway in human endometrial tissues were assessed using western blot analysis. An adenomyosis mouse model was created using 1 mg/kg tamoxifen, followed by treatment with evodiamine and dual antiplatelet therapy (DAPT). Expression levels of alpha-smooth muscle actin (α-SMA), collagen I, neural cadherin (N-cadherin), epithelial cadherin (E-cadherin), Snail, and Vimentin were evaluated using western blot analysis. Immunohistochemistry was used to assess Jagged-1, Notch1, and Hes1 levels. Hematoxylin and eosin (H&E) staining evaluated the depth of endometrial infiltration into the myometrium, and Masson trichrome staining quantified collagen content. Results: The Jagged-1/Notch1/(hairy and enhancer of split 1) Hes1 pathway was found to be activated in the endometrial tissues of adenomyosis patients. In adenomyosis mice, evodiamine treatment led to the inhibition of the Jagged-1/Notch1/Hes1 pathway, along with observable morphological changes, such as reduced adenomyosis nodules with congestion. This improvement was significant compared to the control group (p < 0.05). Furthermore, evodiamine and DAPT treatments reduced endometrial infiltration into the myometrium and collagen deposition while suppressing the expression of α-SMA, collagen I, N-cadherin, Snail, and Vimentin, and upregulating E-cadherin expression. The inhibitory effect was significantly greater than that in the control group (p < 0.05). Conclusion: Evodiamine mitigated adenomyosis by regulating EMT through the inactivation of the Jagged-1/Notch1/Hes1 pathway. This finding suggests that evodiamine could be a potential treatment option for adenomyosis.

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References Supporting Agencies Copyright (c) 2023 Xiaorui Dong, Xixi Chen, Mengling Xue, Yina Zhang This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Medical Genetics, University of Torino Medical School, Italy Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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