Abstract
Endometrial injury is a common female disease. This study was designed to illustrate the effects of oxycodone on mifepristone-induced human endometrial stromal cells (hEndoSCs) injury and delineate the underlying molecular mechanism. hEndoSCs were stimulated with mifepristone to generate the endometrial injury in vitro model. hEndoSCs viability, cytotoxicity, and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay, lactate dehydrogenase assay (LDH), and flow cytometry (FCM) analysis, respectively. Meanwhile, quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blot assay were conducted to evaluate gene and protein expressions. The secretions of inflammatory cytokines (TNF-α, IL-1β, and IL-6) were measured using enzyme-linked immunosorbent assay (ELISA). The data revealed that mifepristone exposure memorably inhibited hEndoSCs viability and promoted cell apoptosis and inflammatory cytokines secretion, and oxycodone had no cytotoxicity on hEndoSCs. Oxycodone increased hEndoSCs growth, blocked cell apoptosis, enhanced Bcl-2 expression, reduced Bax levels, and decreased the secretion of inflammatory cytokines in mifepristone-induced hEndoSCs, exhibiting the protective effects in endometrial injury. In addition, the TLR4/NF-κB pathway-related protein levels (TLR4 and p-p65) in mifepristone-treated hEndoSCs were enhanced, while these enhancements were inhibited by oxycodone treatment. In conclusion, oxycodone exhibited the protective role in mifepristone-triggered endometrial injury via inhibiting the TLR4/NF-κB signal pathway.
Highlights
Endometrial injury is a common female disease. is study was designed to illustrate the effects of oxycodone on mifepristoneinduced human endometrial stromal cells injury and delineate the underlying molecular mechanism. hEndoSCs were stimulated with mifepristone to generate the endometrial injury in vitro model. hEndoSCs viability, cytotoxicity, and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay, lactate dehydrogenase assay (LDH), and flow cytometry (FCM) analysis, respectively
Accumulating evidences have demonstrated that multiple factors including ROS/NLRP3/caspase-1/GSDMD, WNT, and mTOR signaling pathway were involved in the progression of endometrial diseases [10,11,12]. e TLR4/NFκB pathway has been identified to be involved in many diseases
Endometrial Injury Model Was Successfully Established by Mifepristone. hEndoSCs were treated with mifepristone to induce the endometrial injury model in vitro. en, the cell viability, secretion of inflammatory cytokines, and cell apoptosis were detected to evaluate the endometrial injury
Summary
Endometrial injury is a common female disease. is study was designed to illustrate the effects of oxycodone on mifepristoneinduced human endometrial stromal cells (hEndoSCs) injury and delineate the underlying molecular mechanism. hEndoSCs were stimulated with mifepristone to generate the endometrial injury in vitro model. hEndoSCs viability, cytotoxicity, and apoptosis were measured by methyl thiazolyl tetrazolium (MTT) assay, lactate dehydrogenase assay (LDH), and flow cytometry (FCM) analysis, respectively. Oxycodone exhibited the protective role in mifepristone-triggered endometrial injury via inhibiting the TLR4/NF-κB signal pathway. Us, this research was designed to investigate the roles and mechanism of oxycodone in mifepristone-induced hEndoSCs during the pathogenesis of endometrial injury.
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