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Moringa oleifera Seed Extract Alleviates Scopolamine-Induced Learning and Memory Impairment in Mice
Juan Zhou1, Wu-Shuang Yang2, Da-Qin Suo3
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, Xiamen University, Xiamen, China.
Moringa oleifera seed extract (MSE) shows potential as a neuropharmacological drug. It improved memory and learning in mice by enhancing brain cell communication and growth, possibly treating amnesia.
Area of Science:
- Neuropharmacology
- Neuroscience
- Natural Product Research
Background:
- Moringa oleifera seeds possess diverse pharmacological properties.
- Cognitive impairment is often linked to reduced cholinergic activity and neurogenesis.
- Scopolamine is a common agent used to induce amnesia in animal models.
Purpose of the Study:
- To investigate the neuropharmacological effects of Moringa oleifera seed extract (MSE) on scopolamine-induced cognitive impairment in mice.
- To elucidate the mechanisms underlying MSE's effects on memory, cholinergic system, and neurogenesis.
Main Methods:
- Administered 70% ethanolic MSE (250 or 500 mg/kg) orally to mice for 7 or 14 days.
- Induced cognitive impairment using intraperitoneal scopolamine injection (4 mg/kg).
- Assessed cognitive function using passive avoidance and Morris water maze (MWM) tests; analyzed hippocampal cholinergic reactivity, neurogenesis, and key protein expressions (p-Akt, p-ERK1/2, p-CREB).
Main Results:
- Scopolamine injection impaired learning, memory, cholinergic system reactivity, and hippocampal neurogenesis.
- MSE pretreatment significantly reversed scopolamine-induced cognitive deficits.
- MSE enhanced cholinergic neurotransmission and neurogenesis, reversing scopolamine-induced decreases in p-Akt, p-ERK1/2, and p-CREB protein expression in the hippocampus.
Conclusions:
- MSE exhibits potent neuropharmacological effects, ameliorating cognitive impairment in mice.
- The mechanism involves enhancing cholinergic neurotransmission and hippocampal neurogenesis.
- MSE's effects are mediated through the activation of Akt, ERK1/2, and CREB signaling pathways, suggesting its potential as a therapeutic agent for amnesia.
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