Abstract
Enteromorpha prolifera, a green alga, has long been used in food diets as well as traditional remedies in East Asia. Our preliminary study demonstrated that an ethyl acetate extract of Enteromorpha prolifera (EAEP) exhibited the strongest antioxidant activity compared to ethanol or water extracts. Nonetheless, there has been no report on the effect of EAEP on memory impairment due to oxidative damage. This study investigated whether EAEP could attenuate memory deficits in an oxidative stress-induced mouse model. EAEP was orally administered (50 or 100 mg/kg body weight (b.w.)) to mice and then scopolamine was administered. The oral administration of EAEP at 100 mg/kg b.w. significantly restored memory impairments induced by scopolamine, as evaluated by the Morris water maze test, and the passive avoidance test. Further, EAEP upregulated the protein expression of BDNF, p-CREB, p-TrkB, and p-Akt. Moreover, EAEP downregulated the expression of amyloid-β, tau, and APP. The regulation of cholinergic marker enzyme activities and the protection of neuronal cells from oxidative stress-induced cell death in the brain of mice via the downregulation of amyloid-β and the upregulation of the BDNF/TrkB pathway by EAEP suggest its potential as a pharmaceutical candidate to prevent neurodegenerative diseases.
Highlights
As life expectancy increases in humans, the incidence of neurodegenerative disorders in elderly people has increased
Our preliminary study demonstrated that an ethyl acetate extract of Enteromorpha prolifera (EAEP) exhibited the strongest antioxidant activity compared to ethanol or water extracts [34]
In the CA1 region of scopolamine-induced mice treated with EAEP (100 mg/kg), the amount of neuronal degradation was restored to that in normal control mice. These results suggest that EAEP attenuated neuronal injury from oxidative stress induced by scopolamine
Summary
As life expectancy increases in humans, the incidence of neurodegenerative disorders in elderly people has increased. Alzheimer’s disease (AD), one of the most common types of neurodegenerative disorders, is caused by extensive oxidative stress [1,2]. An abnormally excessive accumulation of β-amyloid forms oligomers and plaques that cause a progressive decline in cognition and degeneration of the cholinergic nervous system pathology [4,5]. Disruption of the cholinergic nervous system in the hippocampus and brain cortex reduces the levels of acetylcholine (ACh) and choline acetyltransferase (ChAT), and increases the levels of acetylcholinesterase (AChE), which catalyzes choline esters, leading to memory impairment and behavioral disorders [4,5,6]. Scopolamine, a blocker of muscarinic ACh receptors, is used to induce oxidative stress, reduce hippocampal volume, and dysregulate the cholinergic neuronal pathway in rodents and humans [7,8].
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