Abstract
This study evaluated Moringa oleifera extracts from two locations in Niger Delta for in vitro anti-cholinesterase and antioxidant activities. Methanolic, aqueous and ethanolic extracts of Moringa oleifera were evaluated for inhibition of acetylcholinesterase (AChE) activity, antioxidant properties, and total phenolic and flavonoid contents using standard procedures. M. oleifera extracts possessed significant and concentration dependent AChE inhibitory activity for methanolic, aqueous, and ethanolic extracts. For the most potent extracts, the percentage AChE inhibition/IC50 (µg/mL) values were Moringa oleifera root methanolic extracts (MORME): ~80%/0.00845; Moringa oleifera root ethanolic extract 1 (MOREE1): ~90%/0.0563; Moringa oleifera root ethanolic extract 2 (MOREE2): ~70%/0.00175; and Moringa oleifera bark ethanolic extract (MOBEE): ~70%/0.0173. The descending order of AChE inhibitory potency of plant parts were: root > bark > leaf > flowers > seed. All M. oleifera methanolic extracts at a concentration of 1000 µg/mL displayed significant (p < 0.05–0.001) DPPH radical scavenging activity, with values of ~20–50% of that of ascorbic acid. The total phenolic content and total flavonoid content (TPC/TFC) of MORME, Moringa Oju bark methanolic extract (MOBME), MOREE1, MOREE2 and Moringa leaf ethanolic leaf extract (MLEE) were (287/254), (212/113), (223/185), (203/343) and (201/102) mg gallic acid equivalents/g and quercetin equivalents/g, respectively. There was an inverse correlation between plant extract AChE inhibition and total phenolic (p < 0.0001) and total flavonoid contents (p < 0.0012). In summary, this study revealed 5 of 19 extracts of M. oleifera that have potent in vitro anti-cholinesterase and antioxidant activities.
Highlights
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease and is associated with progressive and irreversible loss of cognitive abilities, memory loss, cognitive impairment, emotional dysfunction, and death [1]
AD is characterized by the formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cerebral cortex of afflicted humans [6,7]
M. oleifera neuroprotective effects have been reviewed [59,60,61,62] and experimentally demonstrated [40,41,63]. Various mechanisms, such as AChE inhibition, modification of monoamine levels, anti-amyloid aggregation, and antioxidant activities are strategies that have been employed for the amelioration of AD symptoms [60]
Summary
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease and is associated with progressive and irreversible loss of cognitive abilities, memory loss, cognitive impairment, emotional dysfunction, and death [1]. The epidemic scale of dementia poses one of the major challenges on global public health systems and associated financial burden. The financial burden, coupled to the social stigma associated with the loss of cognitive abilities and dependency on others, imposes considerable psychological distress in patients as well as their families [5]. AD is characterized by the formation of senile plaques, composed mainly of amyloid β (Aβ), and neurofibrillary tangles (NFTs), composed of tau protein, in the hippocampus and cerebral cortex of afflicted humans [6,7] These protein aggregates (Aβ and tau proteins) provoke neuronal damage and synaptic dysfunction [8,9], the inhibition of their formation remains a potential therapeutic approach for the treatment of AD [10]
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