Journal of Cancer Prevention : pISSN 2288-3649 / eISSN 2288-3657

Fig. 1.

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Fig. 1. Effect of astaxanthin (AST) on mitochondrial reactive oxygen species (ROS), superoxide dismutase (SOD) levels and SOD activity in Helicobacter pylori-infected AGS cells. The cells were pre-treated with 1 or 5 μM of AST for 3 hours and then stimulated with H. pylori for 1 hour. (A) Mitochondrial ROS levels were measured by MitoSOX fluorescence. “None” corresponds to uninfected cells; “Control” corresponds to the cells infected with H. pylori alone; “AST” corresponds to the cells infected with H. pylori with treatment of 5 μM AST. aP < 0.05 vs. “none”; bP < 0.05 vs. “control”. (B) The levels of SOD1 and SOD2 were measured by Western blot analysis for uninfected AGS cells (none), those infected with H. pylori (control), AGS cells infected with H. pylori and treated with 1 or 5 μM AST (left panel). The protein level of SOD1 and SOD2 were compared to that of actin and expressed as the percentage density ratio. All values were expressed as mean ± SE of three different experiments. aP < 0.05 vs. “none”; bP < 0.05 vs. “control” (right panel). (C) SOD activity was measured by a commercial assay kit. The description of the columns is the same as in (A). aP < 0.05 vs. “none”; bP < 0.05 vs. “control”.
J Cancer Prev 2019;24:54-8 https://doi.org/10.15430/JCP.2019.24.1.54
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