Hydroxysafflor yellow A ameliorates homocysteine-induced Alzheimer-like pathologic dysfunction and memory/synaptic disorder
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Updated: May 9, 2026

A11-positive β-amyloid Oligomer Preparation and Assessment Using Dot Blotting Analysis
Published on: May 22, 2018
Ya-Qin Lu1, Yu Luo, Zhong-Fang He
11 Department of Neurology, First Hospital of Lanzhou University , Lanzhou, China .
Abstract:
Homocysteine (Hcy) could induce amyloid β (Aβ) accumulation, synaptic dysfunction, and memory impairment as seen in Alzheimer disease (AD), the most prevalent neurodegenerative disorder, which affects more than 25 million people worldwide. Here we investigated the protective effect of hydroxysafflor yellow A (HSYA) on Hcy-induced Aβ accumulation, synaptic dysfunction, and learning and memory deficits. Rats were randomly divided into four groups: Control group, which received normal saline (NS); Hcy group, which received a daily vena caudalis injection of Hcy (400 μg/kg per day); Hcy+HSYA group, which received the same amount of Hcy plus 6 mg/kg per day HSYA intraperitoneally; and HSYA group, which received 6 mg/kg per day HSYA intraperitoneally for 2 weeks. Results showed that simultaneous supplementation of HSYA significantly attenuated Aβ accumulation, improved synaptic function, and reversed Hcy-induced cognitive impairment. Our data suggest that HSYA might be a promising therapeutic candidate for attenuating Hcy-induced AD-like pathological and behavioral deficits.
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