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

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

  • NPJ Sci Food. 2025 Feb 4;9(1):16. doi: 10.1038/s41538-025-00378-y.
Yaoyi Zhang # 1 Shuai Lv # 2 Pinyuan Huang 1 Lingmin Xiao 1 Nan Lin 3 En Huang 4 5
Affiliations

Affiliations

  • 1 Key Laboratory of Brain Aging and Neurodegenerative Diseases of Fujian Province, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China.
  • 2 Department of Pediatrics, The First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning Province, China.
  • 3 Fujian Key Laboratory of Vascular Aging, Department of Geriatrics, Fujian Institute of Geriatrics, Fujian Clinical Research Center for Senile Vascular Aging and Brain Aging, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
  • 4 Key Laboratory of Brain Aging and Neurodegenerative Diseases of Fujian Province, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China. ehuang0705@fjmu.edu.cn.
  • 5 Scientific Research Center, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian Province, China. ehuang0705@fjmu.edu.cn.
  • # Contributed equally.
Abstract

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, β-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-κB 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-κB pathway-mediated inflammatory response and neuroinflammation.

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