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Enteromorpha prolifera Extract Protects against Scopolamine‐induced Memory Impairment in Mice
Author(s) -
KIM MEE REE,
Baek Seong Yeon,
Li FuYi
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.01976
Subject(s) - morris water navigation task , acetylcholinesterase , choline acetyltransferase , pharmacology , glutathione peroxidase , antioxidant , neuroprotection , chemistry , aché , hippocampus , memory impairment , oxidative stress , hippocampal formation , lipid peroxidation , glutathione , glutathione reductase , superoxide dismutase , medicine , biochemistry , endocrinology , acetylcholine , enzyme , cognition , psychiatry
Enteromorpha prolifera (EP) contains various nutrients and phytochemicals that have been reported to play role in antioxidant activity, hypolipidemic and immunomodulatory. However, the neuroprotective effect of EP has not been reported. The present study examined whether EP ethylacetate extract(EPE) improves memory impairment induced by scopolamine. EPE (50 or 100 mg/kg) was administered orally to mice for 14 days, and then scopolamine (2 mg/kg, i.p.) was administered together with EPE for another 14 days. Memory performance was evaluated using the Morris water maze test and passive avoidance test. Also, brain acetylcholinesterase (AChE) and choline acetyltransferase (ChAT) activities, biomarkers of oxidative stress and the loss of neuronal cells in hippocampus was evaluated by histological examinations. Administration of EPE significantly restored memory impairments induced by scopolamine, as demonstrated by the Morris water maze test (escape latency and number of crossing platform area), and in the passive avoidance test. Treatment with EPE inhibited the AChE activity and increased the ChAT activity in the brain of memory impaired mice induced by scopolamine. Additionally, the administration of EPE significantly prevented the increase in lipid peroxidation and the decrease in GSH levels in brain of mice treated with scopolamine. Also, the EPE treatment restored the activities of antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) to control level. Furthermore, scopolamine‐induced oxidative damage of neurons in hippocampal CA1 and CA3 regions were prevented by EPE treatment. It is suggested that EPE may be a useful for mitigating memory improvement via the regulation of cholinergic marker enzyme activities and the suppression of oxidative damage of neurons in the brain of mice treated with scopolamine.