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• W4292997387 endingPage "096032712211206" @default.
• W4292997387 startingPage "096032712211206" @default.
• W4292997387 abstract "Endometriosis (EMS) is often observed in women of childbearing age and significantly impacts patients' quality of life. Ritodrine is a β2 receptor agonist applied for relaxing the uterine smooth muscle. Its inhibitory effects on inflammation have recently been noted. The present study explored the protective impact of Ritodrine on hypoxia/reoxygenation (H/R)- induced injury in endometrial stromal cells (ESCs). Human ESCs (HESCs) were treated with Ritodrine (0.1, 0.5 μM) for 24 h, followed by exposure to H/R for 6 h. Ritodrine ameliorated H/R-induced higher reactive oxygen species (ROS), declined glutathione (GSH) concentration and increased production of tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and monocyte chemotactic protein 1 (MCP-1) in HESCs. Furthermore, Ritodrine ameliorated the H/R-induced higher nuclear level of nuclear factor κ-B (NF-κB) p65 expression and increased luciferase activity of the NF-κB promoter. In addition, we show that Ritodrine mitigated H/R-induced higher estrogen receptor α (ER-α) expression in HESCs. Interestingly, overexpressing ER-α abolished the regulatory effects of Ritodrine on oxidative stress and the NF-κB pathway-mediated inflammation. Collectively, our data reveal that Ritodrine alleviated H/R-induced injury in ESCs by inhibiting the ER-α/NF-κB pathway." @default.
• W4292997387 created "2022-08-25" @default.
• W4292997387 creator A5007014830 @default.
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• W4292997387 date "2022-01-01" @default.
• W4292997387 modified "2023-10-17" @default.
• W4292997387 title "The protective effects of ritodrine against hypoxia/reoxygenation-induced injury in endometrial stromal cells" @default.
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• W4292997387 doi "https://doi.org/10.1177/09603271221120650" @default.
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