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Humanin Ameliorates Free Fatty Acid-Induced Endothelial Inflammation by Suppressing the NLRP3 Inflammasome.

Authors
  • Li, Wenfeng1
  • Zhang, Dandan1
  • Yuan, Wenjin1
  • Wang, Chenggao1
  • Huang, Qing1
  • Luo, Jun1
  • 1 Department of Cardiology, Ganzhou People's Hospital, No. 18, Meiguan Road, Zhanggong District, Ganzhou, Jiangxi 341000, China. , (China)
Type
Published Article
Journal
ACS Omega
Publisher
American Chemical Society (ACS)
Publication Date
Sep 08, 2020
Volume
5
Issue
35
Pages
22039–22045
Identifiers
DOI: 10.1021/acsomega.0c01778
PMID: 32923762
Source
Medline
Language
English
License
Unknown

Abstract

Cardiovascular disease (CVD) has been considered as a major risk factor of death in recent decades. In CVDs, the NLRP3 inflammasome is important for inflammatory response and vascular damage. Therefore, safe and effective treatments to decrease NLRP3 inflammasome activation are required. Increased levels of free fatty acid (FFA) have been associated with the progression of CVD. Humanin, a kind of mitochondrial-derived peptide, has shown its beneficial effects in different types of cells. However, the roles of humanin in the NLRP3 inflammasome induced by FFA are still unknown. Here, we investigated the molecular mechanisms whereby humanin was found to exert protective effects in human aortic endothelial cells (HAECs) against FFA-caused endothelial injury. Here, treatment with humanin inhibited FFA-induced lactate dehydrogenase release, thereby demonstrating a protective capacity against cell death. Humanin also suppressed oxidative stress by downregulating the expression of reactive oxygen species and NOX2. Notably, humanin reduced NLRP3 and p10 and rescued FFA-induced dysfunction of adenosine monophosphate-activated protein kinase. Consequently, humanin inhibited the expression of IL-1β and IL-18. These results conclude that humanin might be a promising therapeutic agent for CVD. Copyright © 2020 American Chemical Society.

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