Sesamin Enhances Nrf2-Mediated Protective Defense against Oxidative Stress and Inflammation in Colitis via AKT and ERK Activation

Figure 1

SSM protected Caco-2 cells from H₂O₂-induced cytotoxicity via GSH-mediated ROS scavenging. (a) Chemical structure of SSM. (b) Caco-2 cells were treated with 0 μM SSM (0.1% DMSO) and various concentrations of SSM (5, 10, 20, 40, 80, 160, and 320 μM) for 8, 16, and 24 h. Cell viability was measured by MTT assay. (c) Caco-2 cells were pretreated with 0 μM SSM (0.1% DMSO) or 40 μM SSM for 2, 4, and 8 h and then treated with various concentrations of H₂O₂ (0, 0.26, 0.6, 0.76, 1.0, 1.26, 1.6, 1.76, and 2.0 mM) for 24 h. Cell viability was measured by MTT assay. (d) Caco-2 cells were pretreated with 0 μM SSM (0.1% DMSO) and various concentrations of SSM (5, 10, 20, 40, and 80 μM) for 8 h and then treated with 1.6 mM H₂O₂ for 24 h. Intracellular ROS were detected using DCFH-DA fluorescence assay. Roseup was used as a positive control (+). Images are displayed at 200x magnification. The quantification of fluorescence was performed with a Flex Station 3 multifunctional microplate reader. Data were expressed as the (). versus the control group. ^# and ^### versus the H₂O₂ treatment group. (e, f) Caco-2 cells were treated with 0 μM SSM (0.1% DMSO) and various concentrations of SSM (10, 20, 40, and 80 μM) for 8 h. Reduced GSH (GSH) and oxidized GSH (GSSG) were detected using commercial kits. Data were expressed as the (). versus the DMSO treatment group. (g) Caco-2 cells were pretreated with 0.1% DMSO (control) or 10 μM BSO and 0 μM SSM (0.1% DMSO) or various concentrations of SSM (5, 10, 20, 40, and 80 μM) for 2 and 8 h, respectively, and then treated with 1.6 mM H₂O₂ for 24 h. Cell viability was measured by MTT assay. Data were expressed as the (). and versus the H₂O₂ treatment group. ^## and ^### versus the control group.

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