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GLP-1 alleviates NLRP3 inflammasome-dependent inflammation in perivascular adipose tissue by inhibiting the NF-κB signalling pathway

Authors
  • Chen, Xiangheng1
  • Huang, Qiuling1
  • Feng, Juling2
  • Xiao, Zhongsheng1
  • Zhang, Xiaoling1
  • Zhao, Lei1
  • 1 Department of Gastrointestinal Surgery, The First Affiliated Hospital, University of South China, Hengyang, China
  • 2 Research Lab of Translational Medicine, Heng Yang Medical School, University of South China, Hengyang, China
Type
Published Article
Journal
The Journal of International Medical Research
Publisher
SAGE Publications
Publication Date
Feb 27, 2021
Volume
49
Issue
2
Identifiers
DOI: 10.1177/0300060521992981
PMID: 33641439
PMCID: PMC7917887
Source
PubMed Central
Keywords
License
Unknown

Abstract

Objectives To study the effect of glucagon-like peptide 1 (GLP-1) on NLR family pyrin domain containing 3 (NLRP3) inflammasome-induced inflammation in perivascular adipose tissue (PVAT) of Zucker diabetic fatty (ZDF) rats and the underlying role of nuclear factor (NF)-κB signalling. Methods Thirty ZDF rats were randomly divided into three study groups: DM (0.9% saline, subcutaneously); DM+GLP-1 (liraglutide, s.c.); and NF-κB+GLP-1 (betulinic acid then liraglutide, s.c.). Ten Zucker lean rats were examined as normal controls. PVAT from ZDF (DM) rats was examined for inflammasome mRNA. Protein levels of NLRP3, cleaved caspase-1, caspase-1, gasdermin D (GSDMD), interleukin (IL)-1β and IL-18 in PVAT were compared between control, DM and DM+GLP-1 groups. Protein levels of NLRP3, IL-1β, IL-18 and NF-κB in PVAT were compared between control, DM, DM+GLP-1 and NF-κB+GLP-1 groups. Results The inflammasome most abundantly expressed in ZDF rat PVAT was NLRP3 . NLRP3, cleaved caspase-1, IL-1β, IL-18, and GSDMD were markedly upregulated in DM versus control tissue, and GLP-1 reversed this effect. Inhibition of NLRP3 inflammasome-associated inflammation by GLP-1 was lost by activation of NF-κB with betulinic acid. Conclusion GLP-1 may alleviate NLRP3 inflammasome-dependent inflammation in PVAT by inhibiting NF-κB signalling.

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