Abstract
Soy (Glycine Max Merr, family Leguminosae) has been reported to possess anti-cancer, anti-lipidemic, estrogen-like, and memory-enhancing effects. We investigated the memory-enhancing effects and the underlying mechanisms of soyasaponin I (soya-I), a major constituent of soy. Impaired learning and memory were induced by injecting ibotenic acid into the entorhinal cortex of adult rat brains. The effects of soya-I were evaluated by measuring behavioral tasks and neuronal regeneration of memory-deficient rats. Oral administration of soya-I exhibited significant memory-enhancing effects in the passive avoidance, Y-maze, and Morris water maze tests. Soya-Ι also increased BrdU incorporation into the dentate gyrus and the number of cell types (GAD67, ChAT, and VGluT1) in the hippocampal region of memory-deficient rats, whereas the number of reactive microglia (OX42) decreased. The mechanism underlying memory improvement was assessed by detecting the differentiation and proliferation of neural precursor cells (NPCs) prepared from the embryonic hippocampus (E16) of timed-pregnant Sprague-Dawley rats using immunocytochemical staining and immunoblotting analysis. Addition of soya-Ι in the cultured NPCs significantly elevated the markers for cell proliferation (Ki-67) and neuronal differentiation (NeuN, TUJ1, and MAP2). Finally, soya-I increased neurite lengthening and the number of neurites during the differentiation of NPCs. Soya-Ι may improve hippocampal learning and memory impairment by promoting proliferation and differentiation of NPCs in the hippocampus through facilitation of neuronal regeneration and minimization of neuro-inflammation.
Highlights
Many patients with various neurological diseases, including Alzheimer’s disease (AD), Parkinson’s disease, epilepsy, depression, and cerebral ischemia, suffer from variable degrees of learning and memory impairment [1,2]
The model rats were generated by stereotaxic microinjection of ibotenic acid (IBO) into the entorhinal cortex of adult male rats as described previously [25,26,27,28,35,36]
We found that cholinergic neurons, which was increased at 1 week after soyasaponin I (soya-I) administration, were maintained at a similar level (Figure 3G) until 4 weeks after administration (Sham n = 5, IBO n = 5, Soya-I 10 mg·kg-1 n = 5; F2,12 = 15.78, p = 0.0004 by One-way analysis of variance (ANOVA); Figure 5D, E), when total endogenous ChAT-positive cells were immunostained, suggesting that administration of soya-I may neuroprotect cholinergic neurons from degeneration induced by IBO injection
Summary
Many patients with various neurological diseases, including Alzheimer’s disease (AD), Parkinson’s disease, epilepsy, depression, and cerebral ischemia, suffer from variable degrees of learning and memory impairment [1,2]. Some neuronal loss may be replaced by adult neurogenesis in the subventricular zone (SVZ) of the lateral ventricle and in the subgranular zone (SGZ) of the hippocampus. In case of AD patients, neuro-degeneration is indicated by serious neuronal cell death in the cerebral cortex and hippocampus. It is caused by depositions of posttranslationally misprocessed proteins, such as β-amyloid and tau, that are found in senile plaques and neurofibrillary tangles. This process is accompanied by memory loss and abnormal behavior. Defects in neurogenesis, including proliferation and differentiation of NPCs may accelerate neuronal loss in the brain of AD patients [2,3,4]
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