Astaxanthin Prevents Decreases in Superoxide Dismutase 2 Level and Superoxide Dismutase Activity in Helicobacter pylori -infected Gastric Epithelial Cells
increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent -associat...
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Published in | Journal of cancer prevention Vol. 24; no. 1; pp. 54 - 58 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
대한암예방학회
01.03.2019
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Subjects | |
Online Access | Get full text |
ISSN | 2288-3649 2288-3657 |
DOI | 10.15430/JCP.2019.24.1.54 |
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Summary: | increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent
-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether
decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in
-infected gastric epithelial AGS cells.
AGS cells were pre-treated with astaxanthin for 3 hours prior to
infection and cultured for 1 hour in the presence of
. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence.
decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by
infection. Astaxanthin prevented
-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells.
Consumption of astaxanthin-rich food may prevent the development of
-associated gastric disorders by suppressing mitochondrial oxidative stress. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2288-3649 2288-3657 |
DOI: | 10.15430/JCP.2019.24.1.54 |