Glycyrrhizic Acid Protects Glomerular Podocytes Induced by High Glucose by Modulating SNARK/AMPK Signaling Pathway.


Journal

Current medical science
ISSN: 2523-899X
Titre abrégé: Curr Med Sci
Pays: China
ID NLM: 101729993

Informations de publication

Date de publication:
Aug 2023
Historique:
received: 02 12 2022
accepted: 19 04 2023
medline: 23 8 2023
pubmed: 14 7 2023
entrez: 14 7 2023
Statut: ppublish

Résumé

Diabetic nephropathy is one of the most important microvascular complications of diabetes, which mainly refers to glomerular capillary sclerosis. Podocytes are an important part of glomerular capillaries. Previous clinical and basic studies have shown that fibrosis is the main factor of diabetic nephropathy. This study aimed to assess the protective mechanism of glycyrrhizic acid (GA) on glomerular podocytes induced by high glucose as we hypothesized that GA may have antifibrotic and anti-inflammatory effects on podocytes through regulation of the adenosine 5'-monophosphate-activated protein kinase (AMPK)/sucrose nonfermenting AMPK-related kinase (SNARK) signaling pathway. SNARK siRNA was used to transfect podocytes. Real-time quantitative polymerase chain reaction and immunofluorescence staining assays were used for molecular and pathological analysis. The expression levels of key pathway proteins (including TGF-β1, α-SMA, SITR1, AMPKα, LKB1, PGC-1α, NF-κB, IL-6, and TNF-α) were verified by Western blotting. The expression of inflammatory factors in podocytes was detected by ELISA. We demonstrated that GA decreased the expression of podocyte fibrosis signaling pathway-related factors by upregulating the AMPK pathway and its related factors. However, after transfection of podocytes with SNARK siRNA, there was an increased expression of fibrosis-related factors and inflammation-related factors. GA can protect podocytes and alleviate fibrosis and inflammation induced by high glucose, which is related to the AMPK signaling pathway. Meanwhile, knockdown of SNARK protein can inhibit the AMPK signaling pathway, aggravate fibrosis, and increase inflammation.

Identifiants

pubmed: 37450070
doi: 10.1007/s11596-023-2765-y
pii: 10.1007/s11596-023-2765-y
doi:

Substances chimiques

AMP-Activated Protein Kinases EC 2.7.11.31
Glucose IY9XDZ35W2
Glycyrrhizic Acid 6FO62043WK
RNA, Small Interfering 0
SNARK protein, mouse EC 2.7.11.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

696-707

Informations de copyright

© 2023. Huazhong University of Science and Technology.

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Auteurs

Tian-Qi Zhao (TQ)

School of Basic Medicine, Ningxia Medical University, Yinchuan, 750004, China.

Yuan Li (Y)

School of Nursing, Ningxia Medical University, Yinchuan, 750004, China.

Miao Zhang (M)

Department of Pathology, People's Hospital of Ningxia Hui Autonomous Region, Yinchuan, 750004, China.

Meng-Chao Zhao (MC)

Department of Pharmacy, General Hospital of Ningxia Medical University, Yinchuan, 750004, China.

Xue Cao (X)

School of Basic Medicine, Ningxia Medical University, Yinchuan, 750004, China.

Shao-Zhang Hou (SZ)

School of Basic Medicine, Ningxia Medical University, Yinchuan, 750004, China. houshzh@nxmu.edu.cn.

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