In:
PLOS ONE, Public Library of Science (PLoS), Vol. 18, No. 9 ( 2023-9-1), p. e0291022-
Abstract:
Recently, myocardial ischemia-reperfusion (I/R) injury was suggested associated with intestinal flora. However, irisin has demonstrated beneficial effects on myocardial I/R injury, thus increasing interest in exploring its mechanism. Therefore, whether irisin interferes in gut microbiota and gut mucosal barrier during myocardial I/R injury was investigated in the present study. Irisin was found to reduce the infiltration of inflammatory cells and fracture in myocardial tissue, myocardial enzyme levels, and the myocardial infarction (MI) area. In addition, the data showed that irisin reverses I/R-induced gut dysbiosis as indicated by the decreased abundance of Actinobacteriota and the increased abundance of Firmicutes, and maintains intestinal barrier integrity, reduces metabolic endotoxemia, and inhibits the production of proinflammatory cytokines interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α). Based on the results, irisin could be a good candidate for ameliorating myocardial I/R injury and associated diseases by alleviating gut dysbiosis, endothelial dysfunction and anti-inflammatory properties.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0291022
DOI:
10.1371/journal.pone.0291022.g001
DOI:
10.1371/journal.pone.0291022.g002
DOI:
10.1371/journal.pone.0291022.g003
DOI:
10.1371/journal.pone.0291022.g004
DOI:
10.1371/journal.pone.0291022.g005
DOI:
10.1371/journal.pone.0291022.g006
DOI:
10.1371/journal.pone.0291022.g007
DOI:
10.1371/journal.pone.0291022.g008
DOI:
10.1371/journal.pone.0291022.g009
DOI:
10.1371/journal.pone.0291022.s001
DOI:
10.1371/journal.pone.0291022.s002
DOI:
10.1371/journal.pone.0291022.s003
DOI:
10.1371/journal.pone.0291022.s004
DOI:
10.1371/journal.pone.0291022.s005
DOI:
10.1371/journal.pone.0291022.r001
DOI:
10.1371/journal.pone.0291022.r002
DOI:
10.1371/journal.pone.0291022.r003
DOI:
10.1371/journal.pone.0291022.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2023
detail.hit.zdb_id:
2267670-3
Permalink