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ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Renal Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1560420
This article is part of the Research TopicCell Death in Kidney Diseases: Novel Biomarkers, Mechanisms, and Therapeutic StrategiesView all 15 articles
Integrating proteomics and network pharmacology to explore the relevant mechanism of Huangkui capsule in the treatment of chronic glomerulonephritis
Provisionally accepted- 1China Pharmaceutical University, Nanjing, China
- 2Suzhong Pharmaceutical Group Co., Ltd., Taizhou, China
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By integrating proteomics and network pharmacology (NP), we employed a comprehensive approach to elucidate the therapeutic mechanism of Huangkui capsule (HKC) in the treatment of Chronic Glomerulonephritis (CGN). Utilizing LC-MS, we investigated the active components of HKC, while inducing CGN in rats and administering therapeutic drugs. In the rats, we assessed kidney-related indicators and serum inflammatory factors. Histopathological changes in the kidneys were observed through Hematoxylin-eosin staining (HE), and IgG deposition was visualized via immunofluorescence. Through a combined analysis of proteomics and network pharmacology, we examined the targeted effects of HKC on CGN treatment. Our study identified 39 compounds within HKC and demonstrated its significant improvement in glomerulopathy severity in rats. Proteomics analysis revealed 2079 differential proteins in renal tissues, primarily associated with oxidoreductase activity. Network pharmacology investigation uncovered 462 targets associated with HKC and 1835 targets related to CGN. Among them, 13 targets were identified, and subsequent examinations confirmed that HKC effectively reduced STAT3, PIK3R1, AKT1, HIF-1α, and VEGF levels in renal tissue. In summary, HKC ameliorates renal function indicators in CGN rats by modulating HIF-1α, VEGF, PI3K-Akt, MAPK, PPAR, and other signaling pathways. It attenuates inflammatory and oxidative responses, mitigates
Keywords: Huangkui Capsule, Proteomics, Network Pharmacology, Chronic glomerulonephritis, Mechanism
Received: 14 Jan 2025; Accepted: 16 Apr 2025.
Copyright: © 2025 Wen, zou, li, wang and ge. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
fujiang wang, Suzhong Pharmaceutical Group Co., Ltd., Taizhou, China
haitao ge, Suzhong Pharmaceutical Group Co., Ltd., Taizhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.