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Mechanisms of calamus chinensis-chuanxiong ameliorating Alzheimer’s disease by regulating the Nrf2/HO-1 pathway
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DOI   10.11656/j.issn.1673-9043.2025.08.07
Key Words   calamus;chuanxiong;Alzheimer’s disease;oxidative stress;Nrf2/HO-1 signaling pathway
Author NameAffiliationE-mail
SU Linlin Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
LIANG Bing Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
XU Haiying Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
GUO Lichen Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
CAO Yushuang Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
DU Xinyuan Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
ZHANG Tong Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China  
YUAN Qing Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Component Chinese Medicines, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China 
yuanxqing@tjutcm.edu.cn 
HU Limin Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
State Key Laboratory of Component Chinese Medicines, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China
Key Laboratory of Pharmacology of Chinese Medicines, Tianjin 301617, China 
hulimin@tjutcm.edu.cn 
Abstract
    [Objective] To investigate the effects of water extract of acorus tatarinowii and ligusticum chuanxiong(SCP-CX) on anti-oxidative stress and cognitive function in mice with Alzheimer’s disease(AD) induced by D-galactose-sodium nitrite(D-gal—NaNO2). [Methods] Eight-month-old C57BL/6 mice were randomly divided into Control group,Model group,and drug administration group(Donepezil group(0.5 mg/kg),SCP group(1.6 mg/kg),CX group(0.8 mg/kg) and SCP-CX group(1.6 mg/kg vs. 0.8 mg/kg),each group with 10 mice. AD model mice were established by subcutaneous injection of D-gal—NaNO2 for 12 consecutive weeks,and the drug was administered by gavage starting after the 4th week of modeling. The learning and spatial memory abilities of mice were evaluated by Morris water maze experiment,the serum levels of glutathione peroxidase(GSH-PX),malondialdehyde(MDA) and superoxide dismutase(SOD) activities of mice were detected by the kit,and the levels of reactive oxygen species(ROS) and β-amyloid1-40(Aβ1-40) in the hippocampal area of mouse brain tissue were determined by ELISA,and the protein expression of nuclear factor-erythroid 2 related factor 2(Nrf2),heme oxygenase 1(HO-1) in mouse brain tissue was detected by Western Blotting. [Results] Compared with the Model group,the escape latency was significantly shorter(P<0.05) and the number of ascending plateaus increased(P<0.05) in each dosing group;GSH-Px levels were significantly increased(P<0.05);SOD activity was significantly decreased(P<0.05);ROS levels were significantly reduced(P<0.05);and Aβ1-40 deposition was significantly reduced(P<0.05). Compared with the Model group,the SCP-CX group could significantly increase Nrf2 and HO-1 protein expression(P<0.05);compared with the SCP group,the SCP-CX group was able to significantly increase Nrf2 protein expression(P<0.05). [Conclusion] SCP-CX can improve cognitive dysfunction in AD model mice by modulating the Nrf2/HO-1 signaling pathway to reduce oxidative stress and Aβ deposition in the mouse brain.

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