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Integrating network pharmacology and component analysis to investigate the potential mechanisms of Sheng-Hui-Yi-Zhi decoction in the treatment of Alzheimer’s disease

莫里斯水上航行任务 海马体 汤剂 蛋白激酶B 药理学 MAPK/ERK通路 污渍 p38丝裂原活化蛋白激酶 中医药 医学 心理学 化学 神经科学 细胞凋亡 信号转导 内科学 生物化学 基因 病理 替代医学
作者
Peng Wang,Ying Dong,Shanshan Li,Yi Jin,Weiliang Sun,Baosheng Zhao,Qiu-bing Li,Xin Chen
出处
期刊:Journal of Alzheimer's Disease [IOS Press]
标识
DOI:10.1177/13872877241305744
摘要

Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment. Objective To elucidate the potential mechanisms of Sheng-Hui-Yi-Zhi (SHYZ) for the treatment of AD and explore the effective substances of SHYZ. Methods Liquid chromatography-mass spectrometry (LC-MS) was used to identify the active components of SHYZ. Network pharmacology was employed to predict the potential targets and pathways of SHYZ in the treatment of AD. SAMP8 mice were used as a model for AD and were treated with SHYZ. The Morris water maze was utilized to assess the learning and memory capabilities of mice. Additionally, the levels of TNF-α, IL-1β, and IL-6 in the brain hippocampus of mice were quantified using ELISA. The protein expression of PI3 K/p-PI3 K, AKT/p-AKT, MAPK38/p-MAPK38, and NFκB p65/p-NFκB p65 in the hippocampus was analyzed using Western blotting. Additionally, qRT-PCR was employed to assess the gene expressions of TNF-α, IL-1β, and IL-6 in the hippocampus. Result The network pharmacological prediction results showed that the treatment of AD with SHYZ was closely related to the inhibition of inflammatory response. Behavioral experiments revealed that SHYZ significantly reduced the time taken to escape, increased the number of times the platform was crossed, and prolonged the residence time in the target quadrant. Meanwhile, SHYZ treatment suppressed the expression of Aβ 1−42 protein and inflammatory factors. SHYZ significantly inhibited the expression of proteins of PI3 K, AKT, MAPK p38, and NF-κB p65. Conclusions SHYZ has been shown to effectively ameliorate learning and memory impairment in SAMP8 AD mice by inhibiting the expression of Aβ 1−42 and reducing the increase of inflammatory factors.

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