Abstract
The extract of Moringa oleifera seeds has been shown to possess various pharmacological properties. In the present study, we assessed the neuropharmacological effects of 70% ethanolic M. oleifera seed extract (MSE) on cognitive impairment caused by scopolamine injection in mice using the passive avoidance and Morris water maze (MWM) tests. MSE (250 or 500 mg/kg) was administered to mice by oral gavage for 7 or 14 days, and cognitive impairment was induced by intraperitoneal injection of scopolamine (4 mg/kg) for 1 or 6 days. Mice that received scopolamine alone showed impaired learning and memory retention and considerably decreased cholinergic system reactivity and neurogenesis in the hippocampus. MSE pretreatment significantly ameliorated scopolamine-induced cognitive impairment and enhanced cholinergic system reactivity and neurogenesis in the hippocampus. Additionally, the protein expressions of phosphorylated Akt, ERK1/2, and CREB in the hippocampus were significantly decreased by scopolamine, but these decreases were reversed by MSE treatment. These results suggest that MSE-induced ameliorative cognitive effects are mediated by enhancement of the cholinergic neurotransmission system and neurogenesis via activation of the Akt, ERK1/2, and CREB signaling pathways. These findings suggest that MSE could be a potent neuropharmacological drug against amnesia, and its mechanism might be modulation of cholinergic activity via the Akt, ERK1/2, and CREB signaling pathways.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by deterioration of cognitive and behavior function due to cholinergic nervous system dysfunction (Scarpini et al, 2003)
We assessed the effects of M. oleifera seed extract (MSE) on scopolamine-induced cognitive dysfunction using the step-through passive avoidance task
Our results demonstrated that MSE is able to protect mice from scopolamine-induced learning and memory dysfunction as assessed by the passive avoidance and Morris water maze (MWM) tests
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease characterized by deterioration of cognitive and behavior function due to cholinergic nervous system dysfunction (Scarpini et al, 2003). As primarily observed in patients with AD, decreased cholinergic function in the brain can lead to a decline in memory and cognitive function (Hasselmo, 2006). A number of cholinergic drugs have been approved to treat or ameliorate AD, and they exert therapeutic effects. MSE Ameliorates Cognitive Function by preventing acetylcholine (ACh) insufficiency and increasing ACh levels in the brain (Drever et al, 2007). The number of drugs approved for the treatment of AD patients with cognitive impairment is limited due to their side effects, which include pain, nausea and hepatotoxicity (Lahiri et al, 2003). An alternative treatment strategy for AD patients is required
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