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Current Alzheimer Research

Author(s): Xia Jiang*, Lin Chen, Qing Fu, Dan Li Ma, Xue Ting Liu and Xiao Yi Wang

DOI: 10.2174/1567205020666230512094230

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Kidney Yang Deficiency Syndrome Exacerbates Aβ25-35-Induced Pathological Changes, and Ginsenoside Re Ameliorates Synapse Lesions in Aβ25-35- Injected Rats with Kidney Yang Deficiency Syndrome

Page: [48 - 58] Pages: 11

  • * (Excluding Mailing and Handling)

Abstract

Background: Traditional Chinese medicine (TCM) indicates that Alzheimer's disease (AD) is considered the consequence produced by Kidney Yang Deficiency Syndrome (KDS-Yang), which has similar clinical characteristics to glucocorticoid withdrawal syndrome. Ginsenoside Re (G-Re) has been found to ameliorate the symptoms and pathological impairments of AD. However, it’s not clear whether G-Re could protect memory and synapse lesions against kidney deficiency dementia.

Methods: Subcutaneous injection of hydrocortisone for 14 days was used to produce KDS-Yang. On the 15th day, Aβ25-35 peptide was injected into the intracerebroventricular (icv) of KDS-Yang rats. Spine density was analyzed by Golgi staining and the ultrastructural morphology of the synapse was detected using Transmission Electron Microscopy (TEM). Western blot was used to examine the expression of pS396, pS404, Tau-5, tGSK-3β, pS9GSK-3β, Syt, Syn I, GluA1, GluN2B, PSD93, PSD95, β2-AR and pS346-b2-AR.

Results: Hyperphosphorylation of tau in Aβ25-35-injected rats with KDS-Yang was stronger than in Aβ25-35-injected rats at the sites of Ser396 and Ser404. G-Re improved spatial memory damage detected by Morris water-maze (MWM), enhanced spines density, the thickness of postsynaptic density (PSD) and increased the expression of Syt, Syn I, GluA1, GluN2B, PSD93 and PSD95. Moreover, GRe decreased the hyperphosphorylation of β2-AR at serine 346 in Aβ25-35-injected rats with KDS-Yang.

Conclusion: KDS-Yang might exacerbate AD pathological lesions. Importantly, G-Re is a potential ingredient for protecting against memory and synapse deficits in kidney deficiency dementia.

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