Title:New Tiaoxin Recipe Alleviates Energy Metabolism Disorders in an
APPswe/PS1DE9 Mouse Model of Alzheimer’s Disease
Volume: 27
Issue: 4
Author(s): Yiran Hu, Sanli Xing*, Yan Huang, Chuan Chen, Dingzhu Shen and Jiulin Chen
Affiliation:
- Shanghai Geriatric Institute of
Chinese Medicine, Shanghai, 200031, China
Keywords:
Alzheimer’s disease, energy dysmetabolism, new tiaoxin recipe, NAD+, CD38, neurodegenerative disease.
Abstract:
Background: Alzheimer's disease (AD) is a typical neurodegenerative disease with a
complex etiology. Until now, there has been no effective treatment available for AD; however, improving
energy dysmetabolism, the key pathological event in the early stage of AD, can effectively
delay the progression of AD.
Objective: This paper aims to investigate the therapeutic effect and potential mechanism of the new
Tiaoxin recipe on early AD.
Methods: APP/PS1 mice were divided into a model group, a new Tiaoxin recipe group, and a
donepezil group, and C57/BL mice were used for the control group. Mouse cognitive and learning
abilities were tested using the Morris water maze test and a new object-recognition experiment.
The 42 amino acid form of amyloid β peptide (Aβ1–42) content was detected by enzyme-linked
immunosorbent assay, the senile plaque area was detected by thioflavin S staining, and the senescence-
associated β-galactosidase (SA-β-gal)–positive area was detected by chemical staining. Also,
the adenosine triphosphate (ATP), nicotinamide adenine dinucleotide (NAD+), and nicotinamide
adenine dinucleotide hydride (NADH) contents were detected using a biochemical method,
and the cluster of differentiation 38 (CD38) and silent mating–type information regulation 2 homolog
3 (SIRT3) protein expression levels were detected by immunofluorescence and Western blot
analysis.
Results: Compared with those of the control group, the learning and memory abilities of the model
group were impaired; the senile plaque deposition, Aβ1–42 content, and SA-βgal–positive staining
area were increased; the ATP concentration, NAD+ concentration, and NAD+/NADH ratio were
decreased; the CD38 protein expression level was increased; and the SIRT3 protein expression
level was decreased. Following intervention with the new Tiaoxin recipe, the learning and memory
abilities were improved; the senile plaque deposition, Aβ1–42 content, and SA-βgal–positive area
were reduced; the ATP concentration, NAD+ concentration, and NAD+/NADH ratio were increased;
CD38 protein expression was decreased, and SIRT3 protein expression was increased.
Conclusion: This study shows that the new Tiaoxin Recipe can improve cognitive ability and reduce
the Aβ1-42 content and senile plaque deposition in APP/PS1 mice, which may occur through
the downregulation of CD38 protein expression, upregulation of SIRT3 protein expression, restoration
of the NAD+ level, promotion of ATP synthesis, mitigation of energy metabolism disorders.
