Resveratrol protects mesangial cells under high glucose by regulating the miR-1231/IGF1/ERK pathway.

ERK signaling pathway MiR-1231 diabetic nephropathy mesangial cells resveratrol

Journal

Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357

Informations de publication

Date de publication:
29 Dec 2023
Historique:
revised: 13 11 2023
received: 03 10 2023
accepted: 10 12 2023
medline: 29 12 2023
pubmed: 29 12 2023
entrez: 29 12 2023
Statut: aheadofprint

Résumé

Diabetic nephropathy (DN) is one of the complications of diabetes mellitus and the main cause of end-stage renal disease (ESRD), which is a serious threat to human health. In DN, mesangial cells (MCs) are a critical target cell that perform a variety of key functions, and abnormal proliferation of MCs is a common and prominent pathological change in DN. In recent years, the investigation of Chinese medicine interventions for DN has increased significantly in recent years due to the many potential adverse effects and controversies associated with the treatment of DN with Western medicines. In this study, we evaluated the protective effect of resveratrol (RES), an active ingredient known as a natural antioxidant, on HMCs under high glucose and explored its possible mechanism of action. We found that RES inhibited the proliferation of human mesangial cell (HMC) under high glucose and blocked cell cycle progression. In the high glucose environment, RES upregulated miR-1231, reduced IGF1 expression, inhibited the activity of the extracellular signal-regulated kinase (ERK) signaling pathway and reduced levels of the inflammatory factors TNF-α and IL-6. In addition, we found that miR-1231 mimics were synergistically inhibited with RES, whereas miR-1231 inhibitor attenuated the protective effect of RES on HMCs. Thus, our results suggest that the protective effect of RES on HMCs under high glucose is achieved, at least in part, through modulation of the miR-1231/IGF1/ERK pathway. The discovery of this potential mechanism may provide a new molecular therapeutic target for the prevention and treatment of DN, and may also bring new ideas for the clinical research in DN.

Identifiants

pubmed: 38156429
doi: 10.1002/tox.24103
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Tibet Autonomous Region Science and Technology Programme
ID : CGZH2023000195
Organisme : Science and Technology Project from the Education Department of Jilin Province
ID : JJKH20221102KJ
Organisme : Jilin Province Science and Technology Department
ID : 20210101378JC

Informations de copyright

© 2023 Wiley Periodicals LLC.

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Auteurs

Ming Zhang (M)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Yingli Jin (Y)

Department of Pharmacology, School of Basic Medical Science, Jilin University, Changchun, Jilin Province, China.

Xuerui Guo (X)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Wanxin Shan (W)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Jinlong Zhang (J)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Aoxue Yuan (A)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Yan Shi (Y)

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin Province, China.

Classifications MeSH