DOI QR코드

DOI QR Code

Network pharmacology prediction to discover the potential pharmacological action mechanism of Rhizoma Dioscoreae for liver regeneration

  • Wei Liu (College of Basic Medical Sciences, Dalian Medical University) ;
  • Wenyu Wang (Department of Hepatobiliary Surgery, The Second Affiliated Hospital, Dalian Medical University) ;
  • Chenglong Tian (Department of Hepatobiliary Surgery, The Second Affiliated Hospital, Dalian Medical University) ;
  • Ming-Zhong Sun (College of Basic Medical Sciences, Dalian Medical University) ;
  • Shuqing Liu (College of Basic Medical Sciences, Dalian Medical University) ;
  • Qinlong Liu (Department of Hepatobiliary Surgery, The Second Affiliated Hospital, Dalian Medical University)
  • 투고 : 2024.01.03
  • 심사 : 2024.03.09
  • 발행 : 2024.09.01

초록

Improving liver regeneration (LR) remains a medical issue, and there is currently a lack of safe and effective drugs for LR. Rhizoma Dioscoreae (SanYak, SY) is a traditional Chinese medicine. However, the underlying action mechanism of SY treatment for LR is yet to be fully elucidated. To explore the mechanism by which SY affects LR, we have conducted a series of methods for network pharmacological analysis, molecular docking, and in vivo experimental validation in mice. Overall, 9 compounds and 30 predicted target genes of SY were found to be associated with the therapeutic effects of LR. Compared with the model group, hematoxylin and eosin staining revealed that the mice with preoperative drug intervention possessed fewer postoperative hepatocyte bubbles and relatively regular morphology. Furthermore, the serum alanine transaminase and aspartate aminotransferase levels were reduced, immunohistochemistry revealed elevated proliferating cell nuclear antigen positivity rate, and Western blotting demonstrated that the phospho-protein kinase B (AKT)/AKT ratio was downregulated and that vascular endothelial growth factor A (VEGFA) expression levels were upregulated. This study explored dioscin, the main active ingredient of SY, and its potential therapeutic effects on LR. It repairs damaged liver following surgery and promotes liver cell proliferation. The action mechanism comprises reducing AKT phosphorylation levels and upregulating VEGFA expression levels. Thus, this study provides a new direction for further research on the mechanism of SY promoting LR.

키워드

과제정보

This research was funded by the National Natural Science Foundation of China (grant number 81770617).

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