Protective Effect of Yi Shen Pai Du Formula against Diabetic Kidney Injury via Inhibition of Oxidative Stress, Inflammation, and Epithelial-to-Mesenchymal Transition in db/db Mice

Qilin Zhang; Xiaocui Liu; Mitchell A Sullivan; Chen Shi; Bin Deng

doi:10.1155/2021/7958021

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Protective Effect of Yi Shen Pai Du Formula against Diabetic Kidney Injury via Inhibition of Oxidative Stress, Inflammation, and Epithelial-to-Mesenchymal Transition in db/db Mice

Journal article

Open access

Peer reviewed

Protective Effect of Yi Shen Pai Du Formula against Diabetic Kidney Injury via Inhibition of Oxidative Stress, Inflammation, and Epithelial-to-Mesenchymal Transition in db/db Mice

Qilin Zhang, Xiaocui Liu, Mitchell A Sullivan, Chen Shi and Bin Deng

Oxidative Medicine and Cellular Longevity, Vol.2021, pp.1-15

2021

DOI: https://doi.org/10.1155/2021/7958021

PMID: 34504642

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Abstract

Objective. Diabetic kidney disease (DKD) is one of the most common chronic microvascular complications of diabetes; however, there remains a lack of effective therapeutic strategies. Yi Shen Pai Du Formula (YSPDF), a traditional Chinese medicine preparation, has been clinically used in treating chronic kidney disease (CKD) for more than 20 years. However, whether YSPDF has a therapeutic effect on DKD has not been studied. Methods. This study was conducted to investigate the effect of YSPDF administration on db/db mice, a model of type 2 diabetes that develops DKD, and reveal its underlying mechanism of action through a high glucose- (HG-) induced renal injury cell model. Results. We found that YSPDF significantly improved numerous biochemical parameters (fasting blood glucose, serum creatinine, blood urea nitrogen, 24 h urine total protein, total cholesterol, and total triglycerides) and ameliorated the abnormal histology and fibrosis of renal tissue. Moreover, the status of oxidative stress and levels of inflammatory cytokines (TNF-alpha, IL-6, IL-1 beta, and MCP-1) were markedly inhibited by YSPDF treatment. YSPDF treatment significantly mitigated renal fibrosis, with evidence suggesting that this was by inhibiting epithelial-to-mesenchymal transition (EMT) via suppression of the TGF-beta 1/Smad pathway. Interestingly, the expression of Nrf2, HO-1, and NQO1, proteins known to be associated with oxidative stress, were significantly increased upon administration of YSPDF. The levels of NLRP3 inflammasome proteins, including NLRP3, ASC, caspase-1, and cleaved caspase-1 were decreased in the YSPDF-treated group. Cell experiments showed that YSPDF inhibited EMT and the NLRP3 inflammasome in HG-exposed HK-2 cells, possibly via activation of Nrf2. Conclusion. Our study indicates that YSPDF may ameliorate renal damage in db/db mice via inhibition of oxidative stress, inflammation, and EMT, with the mechanism potentially being related to the activation of the Nrf2 pathway.

Details

Title: Protective Effect of Yi Shen Pai Du Formula against Diabetic Kidney Injury via Inhibition of Oxidative Stress, Inflammation, and Epithelial-to-Mesenchymal Transition in db/db Mice
Authors: Qilin Zhang - Huazhong University of Science and Technology
Xiaocui Liu - Hubei University of Medicine
Mitchell A Sullivan - Translational Research Institute
Chen Shi (Corresponding Author) - Huazhong University of Science and Technology
Bin Deng (Corresponding Author) - Huazhong University of Science and Technology
Publication details: Oxidative Medicine and Cellular Longevity, Vol.2021, pp.1-15
Publisher: Hindawi Limited
Date published: 2021
DOI: 10.1155/2021/7958021
ISSN: 1942-0994; 1942-0900
PMID: 34504642
Copyright note: © 2021 Qilin Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Data Availability: The data used to support the findings of this study are available from the corresponding author upon request.
Organisation Unit: School of Health - Biomedicine
Language: English
Record Identifier: 991035094302621
Output Type: Journal article

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Collaboration types: Domestic collaboration; International collaboration
Web Of Science research areas: Cell Biology

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