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基于网络药理学、分子对接和实验验证的20S-原人参二醇对糖尿病肾病潜在靶点的分析

Analysis of potential targets of 20S-protopanaxadiol on diabetic nephropathy based on network pharmacology, molecular docking, and experimental validation.

作者信息

Li Chenfei, Ma Chifa, Zhao Ruxuan, Li Xinfeng, Yu Hengchi, Yuan Mingxia

机构信息

Department of Endocrinology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.

出版信息

Ren Fail. 2025 Dec;47(1):2526688. doi: 10.1080/0886022X.2025.2526688. Epub 2025 Sep 16.

DOI:10.1080/0886022X.2025.2526688
PMID:40957644
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12444918/
Abstract

PURPOSE

This study aims to investigate the protective effects and mechanisms of 20S-protopanaxadiol (PPD), a key component derived from ginseng folium, against diabetic nephropathy (DN).

METHODS

Ingredients of ginseng folium were collected and screened using the TCMSP database. Therapeutic target genes for ginseng folium against DN were obtained, and protein-protein interaction (PPI) networks were constructed. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichments were conducted on these targets. Furthermore, the results of network pharmacology were validated molecular docking. Subsequently,the effects of PPD on TGF-β1/Smads signaling pathway were assessed in db/db mice and HK-2 cells using biochemical assays and Western blotting.

RESULTS

A total of 246 target genes for ginseng folium against DN were identified. KEGG analysis revealed significant enrichment in AGE-RAGE signaling in diabetic complications, PI3K-AKT, MAPK, and TNF pathways. PPD intragastric administration improved renal function in db/db mice and significantly reduced the expression of TGF-β1, α-SMA, p-Smad3, and Smad4 in renal tissue ( < 0.05). Furthermore, PPD decreased the expression of TGF-β1, p-Smad3, and Smad4 in high glucose-induced HK-2 cells.

CONCLUSION

PPD potentially alleviates renal fibrosis in db/db mice and HK-2 cells by inhibiting the TGF-β1/Smads pathway, thereby delaying DN progression.

摘要

目的

本研究旨在探讨人参叶中的关键成分20S-原人参二醇（PPD）对糖尿病肾病（DN）的保护作用及机制。

方法

利用中药系统药理学数据库（TCMSP）收集并筛选人参叶的成分。获取人参叶抗DN的治疗靶点基因，并构建蛋白质-蛋白质相互作用（PPI）网络。对这些靶点进行基因本体论（GO）功能和京都基因与基因组百科全书（KEGG）通路富集分析。此外，通过分子对接验证网络药理学的结果。随后，利用生化分析和蛋白质印迹法评估PPD对db/db小鼠和HK-2细胞中TGF-β1/Smads信号通路的影响。

结果

共鉴定出246个人参叶抗DN的靶点基因。KEGG分析显示，在糖尿病并发症中的AGE-RAGE信号通路、PI3K-AKT、MAPK和TNF通路中显著富集。PPD灌胃给药可改善db/db小鼠的肾功能，并显著降低肾组织中TGF-β1、α-SMA、p-Smad3和Smad4的表达（P<0.05）。此外，PPD可降低高糖诱导的HK-2细胞中TGF-β1、p-Smad3和Smad4的表达。

结论

PPD可能通过抑制TGF-β1/Smads通路减轻db/db小鼠和HK-2细胞的肾纤维化，从而延缓DN的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e80/12444918/0226a3d10637/IRNF_A_2526688_F0010_B.jpg
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