EXPERIMENTAL RESEARCH
A study on inhibition of the Aβ1-42-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway
Su Jiang 1, 2, 3,   Lin-Jie Yu 4,   Hui Yang 5,   Yuexinzi Jin 5,   Jian Chen 4,   Jing-Hua Zhang 5,   Ying Liu 2, 3,   Yun Xu 1, 4, 6
 
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1
Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210008, P. R. China
2
Department of Neurology, Jiangsu Taizhou People’s Hospital, Taizhou, Jiangsu 225300, P. R. China
3
Department of Neurology, Jiangsu Taizhou People’s Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 225300, P. R. China
4
Department of Neurology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, P. R. China
5
Department of Neurology, The Third Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210001, P. R. China
6
Jiangsu Key Laboratory for Molecular Medicine, Nanjing University, Nanjing, Jiangsu 210093, P. R. China
Submission date: 2019-07-05
Final revision date: 2019-09-23
Acceptance date: 2019-10-15
Online publication date: 2020-10-21
 
 
KEYWORDS
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ABSTRACT
Introduction:
The pathology of Alzheimer’s disease (AD) includes -amyloid (A) (plaques) and neurofibrillary tangles (NFTs). This study aimed to explore the efficacy of Huatuo Zaizao pill (HTZP) in an AD mouse model induced by injecting A1-42, and the neuroprotective mechanism of HTZP in AD.

Material and methods:
C57BL/6 (B6) mice were randomly divided into 4 groups (n = 10, per group): control group, AD model group, and 2 different doses of HTZP treated groups. The Morris water maze test was carried out on AD mice to assess the learning ability after treatment with HTZP for 15 day. The levels of inflammatory factors and the nuclear factor-B (NF-B) pathway were examined by western blot and real-time polymerase chain reaction (PCR). The content of microglia was investigated by immunofluorescence.

Results:
This study revealed that a cognitive disorder could be mitigated when the AD mice were treated with HTZP, which might be associated with the decreased level of pro-inflammatory factors, and the inhibitory activities of microglia. Additionally, phosphorylation of IB and NF-B p65 could be reduced by prohibiting the neuroinflammation of NF-B activation in the hippocampus of AD mice.

Conclusions:
These results showed that HTZP could mitigate a cognitive disorder, diminish the activation of microglia, and inhibit the content of inflammatory factors through the NF-B pathway in A1-42-induced AD mice. HTZP may be an appropriate agent for AD treatment in the future.

eISSN:1896-9151
ISSN:1734-1922