Network pharmacology study on the mechanism of berberine in Alzheimer's disease model

被引:0
|
作者
Zhang, Yaoyi [1 ]
Lv, Shuai [2 ]
Huang, Pinyuan [1 ]
Xiao, Lingmin [1 ]
Lin, Nan [3 ]
Huang, En [1 ,4 ]
机构
[1] Fujian Med Univ, Sch Basic Med Sci, Key Lab Brain Aging & Neurodegenerat Dis Fujian Pr, Fuzhou, Fujian, Peoples R China
[2] Dalian Med Univ, Affiliated Hosp 1, Dept Pediat, Dalian, Liaoning, Peoples R China
[3] Fujian Med Univ, Fujian Inst Geriatr, Fujian Clin Res Ctr Senile Vasc Aging & Brain Agin, Dept Geriatr,Fujian Key Lab Vasc Aging,Union Hosp, Fuzhou, Fujian, Peoples R China
[4] Fujian Med Univ, Sci Res Ctr, Sch Basic Med Sci, Fuzhou, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
PREDICTION;
D O I
10.1038/s41538-025-00378-y
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Research indicated that berberine (BBR) plays a protective role in modulating Alzheimer's disease (AD). This study aimed to explore the target genes of BBR associated with AD therapy using a network pharmacology study. Through network pharmacology analysis, two main potential target genes, beta-amyloid precursor protein (APP) and peroxisome proliferator-activated receptor gamma (PPARG), of BBR for AD therapy were screened out. Further experiments demonstrated that BV2 and C8-D1A treated with BBR were decreased in the mRNA and protein expression of APP and presenilin 1 while PPARG was increased with a reduction in the NF-kappa B pathway. A similar result was shown in vivo. Through a network pharmacology study, this study supported that BBR played a protective role in the AD mice model via blocking APP processing and amyloid plaque formation. It also promotes PPARG expression to blockage of NF-kappa B pathway-mediated inflammatory response and neuroinflammation.
引用
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页数:16
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