Protective effect of enzymatic hydrolysates from seahorse (Hippocampus abdominalis) against H2O2-mediated human umbilical vein endothelial cell injury.

Oxidative stress-mediated endothelial dysfunction and LDL oxidation have been implicated in the pathogenesis of atherosclerosis. Thus, the protection of the endothelial cells against oxidative stress-mediated injury and the inhibition of LDL oxidation by the use of antioxidants are a good strategy against atherosclerosis development. Here, we investigated the protective effect and the inhibition of LDL oxidation of seahorse H. abdominalia hydrolysates by Alcalase (SHAH). SHAH showed higher antioxidant activities by measuring DPPH, ABTS+, and ORAC assays than the other hydrolysates. SHAH reduced the formation of thiobarbituric acid reactive substance in Cu2+-induced LDL oxidation. In human umbilical vein endothelial cell (HUVEC), SHAH ameliorated H2O2-mediated HUVEC injury through the restoration of antioxidant enzyme activities and glutathione. In addition, SHAH inhibited HUVEC apoptosis through the down-regulation of caspase-3 and p53 and the increase bcl-2/bax ratio. These results suggested that seahorse H. abdominalia could be developed as potential agents for atherosclerosis.