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
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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