Journal of Alzheimer's disease : JAD · 2025
Integrating network pharmacology and component analysis to investigate the potential mechanisms of Sheng-Hui-Yi-Zhi decoction in the treatment of Alzheimer's disease.
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Wang Peng, Dong Yuan-Li, Li Shan-Shan, Jin Yi, Sun Wei-Liang, Zhao Bao-Sheng, Li Qiu-Bing, Chen Xin
Аннотация
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 Aβ1-42 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 Aβ1-42 and reducing the increase of inflammatory factors.
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 Aβ1-42 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 Aβ1-42 and reducing the increase of inflammatory factors.