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已发表论文
补阳还五汤抑制膜性肾病AGE/RAGE通路的机制：网络药理学整合与细胞模型验证
Authors Fu L, Zhang N, Chen X , Xu X, Shen Y
Received 6 October 2025
Accepted for publication 8 January 2026
Published 17 January 2026 Volume 2026:19 565606
DOI https://doi.org/10.2147/IJGM.S565606
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Professor David E. Stec
Lin Fu,1 Nenghua Zhang,1 Xingying Chen,1 Xiuqin Xu,2 Yunqiu Shen1
1Department of Clinical Laboratory, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, People’s Republic of China; 2Department of Nephrology, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, People’s Republic of China
Correspondence: Lin Fu, Email linfu0725@163.com
Purpose: The Buyang Huanwu Decoction (BYHWD) has demonstrated therapeutic potential in renal-related disorders; however, its pharmacological mechanisms are still poorly understood. Therefore, the aim of this study was to elucidate the regulatory mechanisms of BYHWD in membranous nephropathy (MN).
Methods: Network pharmacology was used to identify BYHWD-related target genes for MN. Enrichment analyses were conducted to determine the relevant biological functions and signaling pathways. An integrated “compound-target-pathway” interaction network was established. The binding affinities between the active compounds and target proteins were determined via molecular docking. Two podocyte injury models were established using zymosan-activated serum (ZAS)-induced MPC-5 cells and Angiotensin II (Ang II)-induced AB8/13 cells. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. ELISA was used to quantify the levels of pro-inflammatory cytokines, membrane attack complexes (MAC, C5b-9), and advanced glycation end products (AGE), while Western blotting was performed to determine receptor for advanced glycation end products (RAGE) protein expression.
Results: BYHWD shared 230 genes with the MN-related targets. GO analysis indicated its involvement in regulating cell proliferation, apoptosis, and inflammation. KEGG analysis highlighted the modulation of the AGE-RAGE signaling pathway. IL-1β showed the highest diagnostic value in the machine learning analysis. Molecular docking revealed stable interactions between key compounds (myristic acid, stigmasterol, quercetin, and β-sitosterol) and target proteins. Both ZAS and Ang II inhibited podocyte proliferation and increased the levels of pro-inflammatory cytokines and C5b-9, whereas BYHWD reversed these effects. It also suppressed AGE and RAGE expression, and these effects were counteracted by pathway agonists.
Conclusion: BYHWD may improve podocyte injury by inhibiting AGE/RAGE and suppressing inflammatory responses and complement activation, providing a preliminary basis for its clinical application.
Keywords: membranous nephropathy, Buyang Huanwu decoction, network pharmacology, AGE/RAGE pathway
1Department of Clinical Laboratory, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, People’s Republic of China; 2Department of Nephrology, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, People’s Republic of China
Correspondence: Lin Fu, Email linfu0725@163.com
Purpose: The Buyang Huanwu Decoction (BYHWD) has demonstrated therapeutic potential in renal-related disorders; however, its pharmacological mechanisms are still poorly understood. Therefore, the aim of this study was to elucidate the regulatory mechanisms of BYHWD in membranous nephropathy (MN).
Methods: Network pharmacology was used to identify BYHWD-related target genes for MN. Enrichment analyses were conducted to determine the relevant biological functions and signaling pathways. An integrated “compound-target-pathway” interaction network was established. The binding affinities between the active compounds and target proteins were determined via molecular docking. Two podocyte injury models were established using zymosan-activated serum (ZAS)-induced MPC-5 cells and Angiotensin II (Ang II)-induced AB8/13 cells. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. ELISA was used to quantify the levels of pro-inflammatory cytokines, membrane attack complexes (MAC, C5b-9), and advanced glycation end products (AGE), while Western blotting was performed to determine receptor for advanced glycation end products (RAGE) protein expression.
Results: BYHWD shared 230 genes with the MN-related targets. GO analysis indicated its involvement in regulating cell proliferation, apoptosis, and inflammation. KEGG analysis highlighted the modulation of the AGE-RAGE signaling pathway. IL-1β showed the highest diagnostic value in the machine learning analysis. Molecular docking revealed stable interactions between key compounds (myristic acid, stigmasterol, quercetin, and β-sitosterol) and target proteins. Both ZAS and Ang II inhibited podocyte proliferation and increased the levels of pro-inflammatory cytokines and C5b-9, whereas BYHWD reversed these effects. It also suppressed AGE and RAGE expression, and these effects were counteracted by pathway agonists.
Conclusion: BYHWD may improve podocyte injury by inhibiting AGE/RAGE and suppressing inflammatory responses and complement activation, providing a preliminary basis for its clinical application.
Keywords: membranous nephropathy, Buyang Huanwu decoction, network pharmacology, AGE/RAGE pathway