LW-AFC, a new formula derived from Liuwei Dihuang decoction, ameliorates behavioral and pathological deterioration via modulating the neuroendocrine-immune abnormalities in PrP-hAβPPswe/PS1ΔE9 transgenic mice
10.3867/j.issn.1000-3002.2017.10.082
- Author:
WANG JIAN-HUI
1
;
LEI XI
;
CHENG XIAO-RUI
;
ZHANG XIAO-RUI
;
LIU GANG
;
CHENG JUN-PING
;
XU YI-RAN
;
ZENG JU
;
ZHOU WEN-XIA
;
ZHANG YONG-XIANG
Author Information
1. Department of Neuroimmunopharmacology
- Keywords:
LW- AFC;
Alzheimer disease;
PrP- hAβPPswe/PS1ΔE9 transgenic mouse;
cognitive behavior;
amyloid-β;
neuron loss;
neuroendocrine;
lymphocyte subset;
cytokine
- From:
Chinese Journal of Pharmacology and Toxicology
2017;31(10):1001-1001
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effect of LW- AFC, a new formula of the main active components extracted from Liuwei Dihuang decoction, on treatment of Alzheimer disease (AD) in mouse models. METHODS After treatment LW- AFC, mice were cognitively evaluated in behavioral experiments. Neuron loss, amyloid-β(Αβ) deposition, and Αβ level were analyzed using Nissl staining, immunofluorescence, and an AlphaLISA assay, respectively. Multiplex bead analysis, a radioimmunoassay, immunochemiluminometry, and an ELISA were used to measure cytokine and hormone levels. Lymphocyte subsets were detected using flow cytometry. RESULTS LW-AFC ameliorated the cognitive impairment observed in APP/PS1 mice, including the impairment of object recognition memory, spatial learning and memory, and active and passive avoidance. In addition, LW-AFC alleviated the neuron loss in the hippocampus, suppressed Αβ deposition in the brain, and reduced the concentration of Aβ1- 42 in the hippocampus and plasma of APP/PS1 mice. LW-AFC treatment also significantly decreased the secretion of corticotropin-releasing hormone and gonadotropin-releasing hormone in the hypothalamus, and adrenocorticotropic hormone, luteinizing hormone, and follicle- stimulating hormone in the pituitary. Moreover, LW-AFC increased CD8+CD28+T cells, and reduced CD4+CD25+Foxp3+T cells in the spleen lymphocytes, down- regulated interleukin(IL)- 1β, IL- 2, IL- 6, IL- 23, granulocyte- macrophage colony stimulating factor, and tumor necrosis factor-α and -β, and up-regulated IL-4 and granulocyte colony stimulating factor in the plasma of APP/PS1 mice. CONCLUSION LW-AFC ameliorated the behavioral and pathological deterioration of APP/PS1 transgenic micevia the restoration of the NIM network to a greater extent than either memantineor donepezil, which supports the use of LW-AFC as a potential agent for AD therapy.
