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

doi:10.1016/j.heliyon.2023.e21997

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 journal › Journal article › peer-review

6 Citations (Scopus)

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 language	English
Article number	e21997
Number of pages	16
Journal	Heliyon
Volume	9
Issue number	11
DOIs	https://doi.org/10.1016/j.heliyon.2023.e21997
Publication status	Published - Nov 2023

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

User-Defined Keywords

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

Access to Document

10.1016/j.heliyon.2023.e21997

Cite this

Liu, H., Chen, W., Tian, C., Deng, Y., Xu, L., Ouyang, W., Qiu, R., You, Y., Jiang, P., Zhou, L., Cheng, J., Kwan, H. Y., Zhao, X., & Sun, X. (2023). The mechanism of Shenbing Decoction II against IgA nephropathy renal fibrosis revealed by UPLC-MS/MS, network pharmacology and experimental verification. Heliyon, 9(11), Article e21997. https://doi.org/10.1016/j.heliyon.2023.e21997

@article{0be831414cde4a48b544253d630fb36b,

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

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.",

keywords = "IgA nephropathy, Network pharmacology, PI3K-Akt signaling pathway, Renal fibrosis, Shenbing Decoction II, TP53",

author = "Huaxi Liu and Weijie Chen and Chunyang Tian and Yijian Deng and Liangwo Xu and Wenkun Ouyang and Renjie Qiu and Yanting You and Pingping Jiang and Lin Zhou and Jingru Cheng and Kwan, \{Hiu Yee\} and Xiaoshan Zhao and Xiaomin Sun",

note = "Funding Information: This work was supported by the National Natural Science Foundation of China, China (81673960, 81774212, 81973666), the Natural Science Foundation of Guangdong Province, China (2018030310451, 2018A0303130320, 2019A1515010400, 2019A1515010816), and the Innovation Team and Talents Cultivation Program of the National Administration of Traditional Chinese Medicine, China. (ZYYCXTD-C-202001). Publisher Copyright: {\textcopyright} 2023 The Authors.",

year = "2023",

month = nov,

doi = "10.1016/j.heliyon.2023.e21997",

language = "English",

volume = "9",

journal = "Heliyon",

issn = "2405-8440",

publisher = "Elsevier BV",

number = "11",

}

TY - JOUR

T1 - The mechanism of Shenbing Decoction II against IgA nephropathy renal fibrosis revealed by UPLC-MS/MS, network pharmacology and experimental verification

AU - Liu, Huaxi

AU - Chen, Weijie

AU - Tian, Chunyang

AU - Deng, Yijian

AU - Xu, Liangwo

AU - Ouyang, Wenkun

AU - Qiu, Renjie

AU - You, Yanting

AU - Jiang, Pingping

AU - Zhou, Lin

AU - Cheng, Jingru

AU - Kwan, Hiu Yee

AU - Zhao, Xiaoshan

AU - Sun, Xiaomin

N1 - Funding Information: This work was supported by the National Natural Science Foundation of China, China (81673960, 81774212, 81973666), the Natural Science Foundation of Guangdong Province, China (2018030310451, 2018A0303130320, 2019A1515010400, 2019A1515010816), and the Innovation Team and Talents Cultivation Program of the National Administration of Traditional Chinese Medicine, China. (ZYYCXTD-C-202001). Publisher Copyright: © 2023 The Authors.

PY - 2023/11

Y1 - 2023/11

N2 - 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.

AB - 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.

KW - IgA nephropathy

KW - Network pharmacology

KW - PI3K-Akt signaling pathway

KW - Renal fibrosis

KW - Shenbing Decoction II

KW - TP53

UR - https://www.scopus.com/pages/publications/85176430366

U2 - 10.1016/j.heliyon.2023.e21997

DO - 10.1016/j.heliyon.2023.e21997

M3 - Journal article

AN - SCOPUS:85176430366

SN - 2405-8440

VL - 9

JO - Heliyon

JF - Heliyon

IS - 11

M1 - e21997

ER -

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

Abstract

UN SDGs

User-Defined Keywords

Access to Document

Other files and links

Fingerprint

Cite this