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MedChemExpress reactive oxygen species ros levels
Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular <t>ROS</t> level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.
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Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular ROS level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Journal: American Journal of Cancer Research

Article Title: Asaraldehyde suppresses non-small cell lung cancer progression via ferroptosis induction and inhibition of PI3K-AKT signaling

doi: 10.62347/UYNG3321

Figure Lengend Snippet: Asaraldehyde inhibits malignant phenotypes of NSCLC through ferroptosis induction. A549 and H1299 cells were treated with various concentrations of Asaraldehyde for 48 h. A. Expression of ferroptosis-related proteins was detected by western blot. B. Intracellular ROS level was detected by DHE staining (magnification, ×100, Scale bar = 50 μm). C. Intracellular labile iron level was detected by FerroOrange staining. (magnification, ×630, Scale bar = 10 μm). D-F. Intracellular GSH, LPO and MDA level were detected by commercial kits. A549, HCC827, H292 and H1299 cells were treated with Asaraldehyde in the presence or absence of 10 µM Ferrostatin-1. G-J. Cell viability was examined by CCK-8 assay. K, L. Colony formation was examined by crystal violet staining. (magnification, ×1, Scale bar = 5 mm). M, N. Cell migration ability was examined by wound healing assay (magnification, ×50, Scale bar = 200 µm). Data were presented as mean ± SD. ns P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: To assess reactive oxygen species (ROS) levels, cells were incubated with 5 μM Dihydroethidium (DHE; MedChemExpress, #HY-D0079) for 30 minutes at 37°C in the dark, then washed twice with PBS.

Techniques: Expressing, Western Blot, Staining, CCK-8 Assay, Migration, Wound Healing Assay