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Archive > Volume 30 Issue 2 > 2023,30(2):123-128. DOI:10.3872/j.issn.1007-385X.2023.02.004 Prev Next
Basic Research
Sesamol regulates autophagy and apoptosis of esophageal squamous cell carcinoma Eca109 cells through AMPK/SIRT1/NF-κB signal pathway
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Abstract:
Objective: To explore the effect of sesamol (SEM) on autophagy and apoptosis of esophageal squamous cell carcinoma (ESCC) Eca109 cells through adenylate activated protein kinase (AMPK)/silencing information regulator 1 (SIRT1)/nuclear factor κB （NF- κB) pathway. Methods: Eca109 cells of ESCC and HEEpiC of human esophageal epithelial cells were treated with different concentrations of SEM (0, 1.562 5, 3.125, 6.25, 12.5, 25, 50, 100, 200, and 400 μmol/L) for 48 hours. Cell viability was detected by CCK-8 method and appropriate SEM concentrations were screened for subsequent experiments. Eca109 cells were grouped into control group (CK group, 0 μmol/L), low-dose SEM group (SEM-L group, 25 μmol/L), medium-dose SEM group (SEM-M group, 50 μmol/L),high-dose SEM group (SEM-M group, 50 μmol/L), high-dose SEM group (SEM-H group, 100 μmol/L) and high-dose SEM+compound C (AMPK inhibitor) group (SEM-H+Compound C group, 100 μmol/L+10 μmol/L). All Eca109 cells were treated at the corresponding drug concentration for 48 hours. CCK-8 assay was applied to detect the proliferation of Eca109 cells; flow cytometry was applied to detect apoptosis; transmission electron microscopy was applied to observe autophagosomes in Eca109 cells and WB assay was applied to detect the protein expressions of microtubule-associated protein 1 light chain 3 (LC3)-Ⅱ/LC3-Ⅰ, Beclin-1, B-lymphoma-2 (Bcl2),Bcl2-associated X protein (BAX), p-AMPK, SIRT1, p-NF-κB p65 in Eca109 cells 2. Results: The SEM concentrations of 25, 50 and 100 μmol/L selected through pre-experiment are used for formal research. Under SEM processing, compared with the CK group, the proliferation levels (24, 48 h) of Eca109 cells, protein expressions of Bcl2 and p-NF-κB p65 in SEM-L group, SEM-M group and SEM-H group decreased significantly while the apoptosis rate, the number of autophagosomes, the protein expressions of LC3Ⅱ-/LC3-Ⅰ,Beclin-1, BAX, p-AMPK and SIRT1 increased significantly, in a dose-dependent manner (all P<0.05); compared with the SEM-H group, the proliferation level (24, 48 h) of Eca109 cells, protein expressions of Bcl2 and p-NF-κB p65 in SEM-H+Compound C group increased significantly while the apoptosis rate, the number of autophagosomes, the protein expressions of LC3Ⅱ-/LC3-Ⅰ, Beclin-1,BAX, p-AMPK and SIRT1 decreased significantly(all P<0.05). Conclusion: SEM may promote autophagy and apoptosis of Eca109 cells by activating AMPK/SIRT1 signaling pathway and inhibiting NF-κB vitality.
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