Soy Isoflavone Alleviates Aß1-42-Induced
Impairment of Learning and Memory Ability
through the Regulation of RAGE/LRP-1
in Neuronal and Vascular Tissue

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:    Frankp@chiro.org

FROM:   Curr Neurovasc Res. 2013 (May); 10 (2): 144—156

Xi YD, Li XY, Ding J, Yu HL, Ma WW, Yuan LH, Wu J, Xiao R.

School of Public Health and Family Medicine,
Capital Medical University,
China, 100069.
xiaor22@ccmu.edu.cn

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The neuroprotective properties of soy isoflavone (SIF) have been demonstrated by our previous studies and others, but its potential mechanism is not clear. Because of the key role of neurovascular dysfunction in the pathogenesis of Alzheimer's disease (AD), we hypothesized neurovascular tissue might be one neuroprotective target of SIF. In the present study, learning and memory ability, ß-amyloid (Aß) expressions both in neurovascular tissue and plasma, the receptor for advanced glycation end products (RAGE), low-density lipoprotein receptor-related protein (LRP)-1, nuclear factor-KB p65 (NF-KB p65), tumor necrosis factor-a (TNF-a) and interleukin-1ß (IL-1ß) expressions in neurovascular tissue were measured in Wistar rats following lateral cerebral ventricle administration of Aß1-42 by miniosmotic pump with or without intragastric administration of SIF from 14 days before surgery to the end of experiment. The results showed that SIF could improve the impairment of learning and memory of rats induced by Aß1-42, maintain Aß homeostasis in brain, regulate the disordered expressions of RAGE/LRP-1 and restrain RAGE related NF-KB and inflammatory cytokines activation in neurovascular structure. These results suggested that soy isoflavone (SIF) could protect Aß-impaired learning and memory in rats, and its mechanism might be associated with the regulation of vascular Aß transportation and vascular inflammatory reaction.

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