Additional file 5 of The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial–mesenchymal transition by phosphorylating β-catenin
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This study established an in vitro oxidative stress model to investigate IL-33 secretion and its effects on cell viability in endometriosis-associated endometrial cells.
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Abstract
Additional file 5: Supplementary Figure 1. Establishment of a Non-lethal Oxidative Stress Model in vitro. A Expression of 4-HNE is in endometrium and ectopic lesions (Scale bars, 20 μm) B-C: Cell viability (B) and fluorescence density (C) of reactive oxygen species (ROS) in ESC treated with different concentration gradients of H2O2. D-F Typical fluorescence picture of ROS(D), expression of malondialdehyde (E), superoxide dismutase, total glutathione peroxidase and catalase (F) in ESC treated with 1μM H2O2. G Secretion of IL-33 at different times after treatment with 1 μM H2O2 in eutopic ESC and ectopic ESC. H Cell lines hESCs, EECs and 12Z were respectively treated with human recombinant IL-33 protein (rIL-33) in vitro at different concentrations (0, 1, 10, 50, 100 ng/ml) and time nodes. Then, the cell viability was determined for the optimal concentration and time parameters of rIL-33 via CCK8. Ctrl-EU, eutopic endometrium of controls; EMs-EU, eutopic endometrium of patients with endometriosis; EMs-EC, ectopic lesions. Data are presented as mean ± SEM. All data were analyzed using one-way ANOVA followed by Dunnett’s post hoc test and Student’s t-test; * p < 0.05, ** p < 0.01, *** p < 0.001.
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