Phlorotannins (marine algal
polyphenols) have been reported to exhibit beneficial biological activities, serving as both
antioxidants and
anti-inflammatory agents. Among marine algae, Ecklonia cava, a member of the Laminariaceae, is a very popular food regarded as healthy in Korea and Japan. Recently, benefits afforded by phlorotannins in the treatment of various clinical conditions have been reported, but any
therapeutic effects of such materials in the treatment of
neurodegenerative diseases such as
stroke remain unclear. Also, the mechanisms of action of the algal components remain poorly understood. In the present in vivo study, administration of Ecklonia cava
polyphenols (ECP)
at 10 mg/kg and 50 mg/kg intraperitoneally (i.p.) significantly decreased
infarct size and the extent of
brain edema in the rat after induction of transient focal
ischemia via
middle cerebral artery occlusion (MCAO). Further,
terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay revealed dose-dependent blockage of neuronal apoptosis upon intravenous ECP treatment. Neurobehavioral tests performed over the 6 days after MCAO revealed a reduction in neurological motor performance in control animals, but administration of ECP (50 mg/kg i.p.) prevented this decline. In vitro, a significant
neuroprotective effect of ECP was evident when cell viability was assayed after induction of H(2)O(2)-mediated oxidative stress, upon
retinoic acid treatment, in the differentiated
neuroblastoma cell line SH-SY5Y. Interestingly, ECP blocked the rise in cytosolic
calcium, in a dose-dependent manner, in differentiated SH-SY5Y cells exposed to H(2)O(2). Together, the results suggest that ECP exerts
neuroprotective effects in the focally ischemic brain by reducing Ca(2+)-mediated neurotoxicity.