Jiang Su, Yu Lin-Jie, Yang Hui, Jin Yuexinzi, Chen Jian, Zhang Jing-Hua, Liu Ying, Xu Yun
Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Department of Neurology, Jiangsu Taizhou People's Hospital, Taizhou, Jiangsu, China.
Arch Med Sci. 2020 Oct 21;19(4):1136-1144. doi: 10.5114/aoms.2020.99427. eCollection 2023.
The pathology of Alzheimer's disease (AD) includes β-amyloid (Aβ) (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 Aβ, and the neuroprotective mechanism of HTZP in AD.
C57BL/6 (B6) mice were randomly divided into 4 groups ( = 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-κB (NF-κB) pathway were examined by western blot and real-time polymerase chain reaction (PCR). The content of microglia was investigated by immunofluorescence.
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 IκB and NF-κB p65 could be reduced by prohibiting the neuroinflammation of NF-κB activation in the hippocampus of AD mice.
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-κB pathway in Aβ-induced AD mice. HTZP may be an appropriate agent for AD treatment in the future.
阿尔茨海默病（AD）的病理学特征包括β-淀粉样蛋白（Aβ）（斑块）和神经原纤维缠结（NFTs）。本研究旨在探讨华佗再造丸（HTZP）对注射Aβ诱导的AD小鼠模型的疗效，以及HTZP在AD中的神经保护机制。
将C57BL/6（B6）小鼠随机分为4组（每组n = 10）：对照组、AD模型组和2个不同剂量的HTZP治疗组。对AD小鼠进行莫里斯水迷宫试验，以评估HTZP治疗15天后的学习能力。通过蛋白质免疫印迹法和实时聚合酶链反应（PCR）检测炎症因子水平和核因子κB（NF-κB）信号通路。通过免疫荧光法研究小胶质细胞的含量。
本研究表明，HTZP治疗可减轻AD小鼠的认知障碍，这可能与促炎因子水平降低和小胶质细胞的抑制活性有关。此外，通过抑制AD小鼠海马中NF-κB激活的神经炎症，可降低IκB和NF-κB p65的磷酸化水平。
这些结果表明，HTZP可减轻Aβ诱导的AD小鼠的认知障碍，减少小胶质细胞的激活，并通过NF-κB信号通路抑制炎症因子的含量。HTZP可能是未来治疗AD的合适药物。
