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Spinosin Attenuates Alzheimer’s Disease-Associated Synaptic Dysfunction via Regulation of Plasmin Activity

Biomolecules & Therapeutics 2020년 28권 2호 p.131 ~ 136
 ( Cai Mudan ) - Kyung Hee University Department of Life and Nanopharmaceutical Sciences

정인호 ( Jung In-Ho ) - Kyung Hee University Department of Life and Nanopharmaceutical Sciences
 ( Kwon Hui-Young ) - Dong-A University College of Health Sciences Department of Medicinal Biotechnology
 ( Cho Eun-Bi ) - Dong-A University College of Health Sciences Department of Medicinal Biotechnology
 ( Jeon Ji-Eun ) - Dong-A University College of Health Sciences Department of Medicinal Biotechnology
윤진호 ( Yun Jean-Ho ) - Dong-A University College of Medicine Department of Biochemistry
이영춘 ( Lee Young-Choon ) - Dong-A University College of Health Sciences Department of Medicinal Biotechnology
김동현 ( Kim Dong-Hyun ) - Dong-A University College of Health Sciences Department of Medicinal Biotechnology
류종훈 ( Ryu Jong-Hoon ) - Kyung Hee University Department of Life and Nanopharmaceutical Sciences

Abstract


Hippocampal synaptic dysfunction is a hallmark of Alzheimer’s disease (AD). Many agents regulating hippocampal synaptic plasticity show an ameliorative effect on AD pathology, making them potential candidates for AD therapy. In the present study, we investigated spinosin as a regulating agent of synaptic plasticity in AD. Spinosin attenuated amyloid β (Aβ)-induced long-term potentiation (LTP) impairment, and improved plasmin activity and protein level in the hippocampi of 5XFAD mice, a transgenic AD mouse model. Moreover, the effect of spinosin on hippocampal LTP in 5XFAD mice was prevented by 6-aminocaproic acid, a plasmin inhibitor. These results suggest that spinosin improves synaptic function in the AD hippocampus by regulating plasmin activity.

키워드

Spinosin; Alzheimer’s disease; Plasmin; LTP; 5XFAD
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