Key result
Pre-treatment with secoisolariciresinol diglucoside abrogated iron-induced increases in oxidative stress, inflammation, and apoptosis in H9c2 cardiomyocytes.
Why the study?
Does secoisolariciresinol diglucoside prevent oxidative stress, inflammation, and apoptosis in an in vitro model of cardiac iron overload?
Does secoisolariciresinol diglucoside prevent oxidative stress, inflammation, and apoptosis in an in vitro model of cardiac iron overload?
Secoisolariciresinol diglucoside (SDG) protects H9c2 cardiomyocytes from iron overload-induced oxidative stress, inflammation, and apoptosis in vitro.
Hypothesis-generating for SDG in iron-overload cardiomyopathy; does not support clinical use and requires in vivo validation.
Cardiac iron overload is directly associated with cardiac dysfunction and can ultimately lead to heart failure. This study examined the effect of secoisolariciresinol diglucoside (SDG), a component of flaxseed, on iron overload induced cardiac damage by evaluating oxidative stress, inflammation and apoptosis in H9c2 cardiomyocytes. Cells were incubated with 50 μ5M iron for 24 hours and/or a 24 hour pre-treatment of 500 μ M SDG. Cardiac iron overload resulted in increased oxidative stress and gene expression of the inflammatory mediators tumor necrosis factor-α, interleukin-10 and interferon γ, as well as matrix metalloproteinases-2 and -9. Increased apoptosis was evident by increased active caspase 3/7 activity and increased protein expression of Forkhead box O3a, caspase 3 and Bax. Cardiac iron overload also resulted in increased protein expression of p70S6 Kinase 1 and decreased expression of AMP-activated protein kinase. Pre-treatment with SDG abrogated the iron-induced increases in oxidative stress, inflammation and apoptosis, as well as the increased p70S6 Kinase 1 and decreased AMP-activated protein kinase expression. The decrease in superoxide dismutase activity by iron treatment was prevented by pre-treatment with SDG in the presence of iron. Based on these findings we conclude that SDG was cytoprotective in an in vitro model of iron overload induced redox-inflammatory damage, suggesting a novel potential role for SDG in cardiac iron overload.
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Puukila et al. (2015) studied Cardiac iron overload. Secoisolariciresinol diglucoside (SDG) vs. Iron treatment alone and untreated control was evaluated on Oxidative stress, inflammation, and apoptosis markers. Pre-treatment with secoisolariciresinol diglucoside abrogated iron-induced increases in oxidative stress, inflammation, and apoptosis in H9c2 cardiomyocytes.
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