Abstract
Platelets have been shown to beneficially respond to plant bioactives, and may undergo oxidative modifications induced by external reactive oxygen species (ROS). Using a human platelet model approach would therefore allow us to assess the efficacy by which plant bioactives affect production of resilience products, and link this to a physiologically relevant outcome, i.e. platelet activation. Human platelets were pre-treated with cinnamaldehyde, curcumin, epigallocatechin gallate, phenethyl isothiocyanate and sulforaphane, all possessing an α, β-unsaturated carbonyl moiety, and challenged with 5 mM H2O2. Platelets were analysed for expression of platelet activation markers, antioxidant enzyme activity, and oxidative stress. Pre-treatment with physiological concentrations of all plant bioactives significantly inhibited ADP-induced P-selectin expression, and thus platelet activation, in a dose response manner, with the concentration of 1 M causing an average inhibition of 7%, and 100 M an average inhibition of 65%. A 5 mM H2O2 oxidative challenge increased platelet P-selectin expression by 13%, but pre-treatment with >25uM of dietary bioactives prevented an increase in platelet activation. In unchallenged platelets, sulforaphane showed pro-oxidant (increased thiobarbituric acid reactive substances (TBARS) by 65%) and phenethyl isothiocyanate (PEITC) anti-oxidant effects (decreased TBARS by 43%). No consistent effects on antioxidant enzyme activities were observed. In conclusion, this study showed that dietary bioactives can maintain platelet function upon exposure to oxidative stress, but it is unclear whether the mechanisms include resilience products - the 5 mM H2O2 challenge may not have been strong enough to enable the detection of the prevention of a rise in levels of SOD and GPx activities. We are currently assessing the effects of an acute combined supplement containing cinnamaldehyde, epigallocatechin gallate and sulforaphane on regulation of baseline antioxidant enzyme activity levels (resilience response) and whether this will prevent an oxidative stress response upon an exhaustive exercise challenge test in healthy subjects.
Published Version
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