The mechanism of Shenbing Decoction II against IgA nephropathy renal fibrosis revealed by UPLC-MS/MS, network pharmacology and experimental verification

Huaxi Liu, Weijie Chen, Chunyang Tian, Yijian Deng, Liangwo Xu, Wenkun Ouyang, Renjie Qiu, Yanting You, Pingping Jiang, Lin Zhou, Jingru Cheng, Hiu Yee Kwan, Xiaoshan Zhao*, Xiaomin Sun*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

Abstract

Background: IgA nephropathy (IgAN) is a major and growing public health problem. Renal fibrosis plays a vital role in the progression of IgAN. This study is to investigate the mechanisms of action underlying the therapeutic effects of Shenbing Decoction II (SBDII) in IgAN renal fibrosis treatment based on ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS), network pharmacology and experimental verification.

Method: We first used UPLC-MS/MS to explore the main compounds of SBDII, and then used network pharmacology to predict the targets and key pathways of SBDII in the treatment of IgAN renal fibrosis. Next, bovine serum albumin (BSA), lipopolysaccharide (LPS), and carbon tetrachloride (CCL4) were used to induce IgAN in rats, and then biochemical indicators, renal tissue pathology, and renal fibrosis-related indicators were examined. At the same time, part of the results predicted by network pharmacology were also verified.

Result: A total of 105 compounds were identified in SBDII by UPLC-MS/MS. Network pharmacology results showed that the active compounds such as acacetin, eupatilin, and galangin may mediate the therapeutic effects of SBDII in treating IgAN by targeting tumor protein p53 (TP53) and regulating phosphatidylinositol 3-kinase (PI3K)-Akt kinase (Akt) signaling pathway. Animal experiments showed that SBDII not only significantly improved renal function and fibrosis in IgAN rats, but also significantly downregulated the expressions of p53, p-PI3K and p-Akt.

Conclusion: This UPLC-MS/MS, network pharmacological and experimental study highlights that the TP53 as a target, and PI3K-Akt signaling pathway are the potential mechanism by which SBDII is involved in IgAN renal fibrosis treatment. Acacetin, eupatilin, and galangin are probable active compounds in SBDII, these results might provide valuable guidance for further studies of IgAN renal fibrosis treatment.

Original languageEnglish
Article numbere21997
Number of pages16
JournalHeliyon
Volume9
Issue number11
DOIs
Publication statusPublished - Nov 2023

Scopus Subject Areas

  • General

User-Defined Keywords

  • IgA nephropathy
  • Network pharmacology
  • PI3K-Akt signaling pathway
  • Renal fibrosis
  • Shenbing Decoction II
  • TP53

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