A study on inhibition of the Aβ1-42-induced inflammatory response by the Huatuo Zaizao pill through the NF-κB signaling pathway

Author:

Jiang Su123,Yu Lin-Jie4,Yang Hui5,Jin Yuexinzi5,Chen Jian4,Zhang Jing-Hua5,Liu Ying23,Xu Yun146

Affiliation:

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

Abstract

IntroductionThe 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 methodsC57BL/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.ResultsThis 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.ConclusionsThese 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.

Publisher

Termedia Sp. z.o.o.

Subject

General Medicine

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