Format

Send to

Choose Destination
Int J Biol Macromol. 2020 Mar 19;154:233-245. doi: 10.1016/j.ijbiomac.2020.03.079. [Epub ahead of print]

Protective effects of chondroitin sulphate nano-selenium on a mouse model of Alzheimer's disease.

Author information

1
Institute of Pharmacology, School of Pharmaceutical Sciences, Shandong Key Laboratory of Cerebral Microcirculation, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian 271000, Shandong, China.
2
Department of Pharmacy, The Second Affiliated Hospital of Shandong First Medical University, Taian 271000, Shandong, China.
3
Institute of Pharmacology, School of Pharmaceutical Sciences, Shandong Key Laboratory of Cerebral Microcirculation, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian 271000, Shandong, China; Department of Pharmacy, Affiliated Hospital of Heze Medical College, Heze 274000, Shandong, China.
4
Institute of Pharmacology, School of Pharmaceutical Sciences, Shandong Key Laboratory of Cerebral Microcirculation, Shandong First Medical University & Shandong Academy of Medical Sciences, Taian 271000, Shandong, China. Electronic address: xiaoyl@sdfmu.edu.cn.

Abstract

In this study, the effect of chondroitin sulphate nano-selenium (CS@Se) on Alzheimer's disease (AD) in mice was investigated. CS@Se alleviated anxiety and improved the spatial learning and memory impairment in AD mice. CS@Se significantly reduced cell oedema and pyknosis, protected the mitochondria, and improved abnormal changes in the ultrastructure of hippocampal neuron synapses of AD mice. Moreover, CS@Se significantly increased the levels of superoxide dismutase(SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase assay (Na+/K+-ATPase) and acetyltransferase (ChAT), and decreased the levels of malondialdehyde (MDA) and acetylcholinesterase (ChAE) in AD mice. Western blot results showed that CS@Se can attenuate excessive phosphorylation of tau (Ser396/Ser404) by regulating the expression of glycogen synthase kinase-3 beta (GSK-3β). In addition, CS@Se can activate the extracellular signal-regulated kinase 1/2 (ERK 1/2) and p38 mitogen-activated protein kinase (p38 MAPK) signalling pathways to inhibit nuclear transcription factor kappa B (NF-κB) nuclear translocation, thereby regulating the expression of pro-inflammatory cytokines. In summary, CS@Se can reduce oxidative stress damage, inhibit excessive tau phosphorylation, reduce inflammation to delay AD development, and increase the learning and memory capacities of AD mice.

KEYWORDS:

Aluminium chloride; Alzheimer's disease; Chondroitin sulphate nano-selenium; D-galactose; Multi-target; Tau

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center