Protective efficacy of an Ecklonia cava extract used to treat transient focal ischemia of the rat brain.
10.5115/acb.2012.45.2.103
- Author:
Jeong Hwan KIM
1
;
Nam Seob LEE
;
Yeong Gil JEONG
;
Je Hun LEE
;
Eun Ji KIM
;
Seung Yun HAN
Author Information
1. Department of Anatomy, Myunggok Research Institute, Konyang University College of Medicine, Daejeon, Korea. jjzzy@konyang.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Ecklonia cava;
Middle cerebral artery infarction;
Neurodegenerative diseases;
SH-SY5Y cells
- MeSH:
Animals;
Anti-Inflammatory Agents;
Antioxidants;
Apoptosis;
Brain;
Brain Edema;
Calcium;
Cell Line;
Cell Survival;
Cytosol;
Infarction, Middle Cerebral Artery;
Ischemia;
Japan;
Korea;
Neuroblastoma;
Neurodegenerative Diseases;
Neurons;
Neuroprotective Agents;
Oxidative Stress;
Polyphenols;
Rats;
Stroke;
Tretinoin
- From:Anatomy & Cell Biology
2012;45(2):103-113
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 H2O2-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 H2O2. Together, the results suggest that ECP exerts neuroprotective effects in the focally ischemic brain by reducing Ca(2+)-mediated neurotoxicity.
