期刊
NEURAL REGENERATION RESEARCH
卷 12, 期 9, 页码 1479-1484出版社
MEDKNOW PUBLICATIONS & MEDIA PVT LTD
DOI: 10.4103/1673-5374.215260
关键词
nerve regeneration; neurodegeneration; genistein; Alzheimer's disease; neuroprotection; hippocampus; learning; memory; tau protein; CAMK4; CALM; CAMKK1; neural regeneration
资金
- National Natural Science Foundation of China [81202941, 81574040]
- Key Project Foundation of Oversea Visiting and Research for the Excellent Young and Middle-aged Faculties in Universities of Anhui Province in China [gxfxZD2016119]
- Key Project Foundation of Natural Science Research in Universities of Anhui Province in China [KJ2016A406]
- Key Project Foundation of Support Program for the Excellent Young Faculties in Universities of Anhui Province in China [gxyq ZD2016138]
Genistein has a neuroprotective effect in Alzheimer's disease, but its mechanism of action needs further clarification. Accumulating evidence suggests that excessive phosphorylation of tau protein causes production of neurofibrillary tangles, which is one of the main pathological characteristics of Alzheimer's disease, and tau protein can be phosphorylated by calcium/ calmodulin dependent protein kinase IV (CAMK4). After 7 days of pre-administration of genistein (90 mg/kg), an Alzheimer's disease rat model was established using an intraperitoneal injection of D-galactose combined with an intracerebral injection of amyloid-beta peptide (25-35). The rat was then continuously administered genistein (90 mg/kg) for 42 days. The Morris water maze test, western blotting and hematoxylin-eosin staining results showed that genistein significantly decreased the escape latency and increased the number of times crossing the platform, reduced p-tau, CALM, CAMKK1 and p-CAMK4 protein levels in the hippocampus, and alleviated hippocampal neuron damage. These findings indicate that genistein may play a neuroprotective role in Alzheimer's disease through regulating CAMK4 to modulate tau hyperphosphorylation.
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