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Mechanism of Yishen Huazhuo Formula in treating Alzheimer’s disease via regulating MAPK/ERK signaling pathway
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DOI   10.11656/j.issn.1673-9043.2025.07.06
Key Words   Alzheimer’s disease;Yishen Huazhuo Formula;cognitive function;synaptic morphology;MAPK/ERK signaling pathway
Author NameAffiliationE-mail
SONG Wanshan Center of Acupuncture and Encephalopathy, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, China  
DAI Ling Center of Acupuncture and Encephalopathy, Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300250, China
Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
WANG Zehui Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
REN Mengyu Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
 
ZHU Jinqiang Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China zhujinqiang1860@163.com 
Abstract
    [Objective] To investigate the mechanism of Yishen Huazhuo Formula(YSHZD) in treating Alzheimer’s disease(AD) through the mitogen-activated protein kinase(MAPK)/extracellular signal-regulated kinase(ERK) signaling pathway. [Methods] Forty male SD rats were randomly divided into sham-operated group(Sham),model group(Model),YSHZD group,and Aricept group(n=10 per group). The AD model was established by intracerebro- ventricular injection of β-amyloid peptide(Aβ25-35). Morris water maze test was performed to evaluate learning and memory abilities. Nissl staining and transmission electron microscopy(TEM) were used to observe neuronal apoptosis and synaptic morphology in the hippocampus,respectively. Western blot was employed to detect the expression of MAPK/ERK pathway-related proteins. [Results] YSHZD significantly improved cognitive function in AD rats,enhanced neuronal survival rate,and protected synaptic ultrastructure. Furthermore,it upregulated the expression of protein kinase C(PKC) and B-Raf proteins,while downregulating Ras,Raf1,and ERK protein levels. [Conclusion] YSHZD ameliorates cognitive dysfunction in AD rats by regulating the MAPK/ERK signaling pathway,thereby promoting neuronal survival and synaptic integrity.

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