Premium
Extracts of purple sweet potato protect pancreatic β‐cells from oxidative stress
Author(s) -
Lin Chia-Yu,
Li Yi-Ying,
Chiang Tzu-Yuan,
Jeng Toong-Long
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.759.9
Subject(s) - oxidative stress , intracellular , antioxidant , reactive oxygen species , toxicity , chemistry , cell , oxidative phosphorylation , diabetes mellitus , cell damage , cell growth , biochemistry , biology , endocrinology , organic chemistry
Pancreatic β‐cells are relatively low in the expression of antioxidant enzymes, which render β‐cells more susceptible to oxidative damage. It has been implied that purple sweet potato (PSP) have anti‐oxidative and anti‐inflammatory effects, as well as may improve blood glucose levels, suggesting the potential benefits of PSP on diabetes. Therefore, the purpose of this study was to investigate the effects of PSP on pancreatic β‐cell protection. INS‐1 cells were treated with PSP and/or H2O2 for different concentrations and different period of time. While H2O2 treatment alone results in a less than 50% viable cells, PSP (10 or 5mg/ml) significantly improves the cell survival in the presence of H2O2 (150μM) toxicity after 24 hours (p<0.05). This recovered cell populations could be due to the enhanced cell proliferation as indicated by BrdU assay. Moreover, the H2O2‐induced intracellular reactive oxygen species generation is partially inhibited by PSP extracts (p<0.05), suggesting the free radical scavenging activity of PSP. The attenuated insulin secretion after H2O2 toxicity is also slightly but significantly rescued by PSP treatment. In summary, these findings indicate that PSP extracts may protect INS‐1 cells from H2O2‐induced oxidative stress and therefore improve cell survival and function.