Sacubitril/valsartan (LCZ696) reduces myocardial injury following myocardial infarction by inhibiting NLRP3‑induced pyroptosis via the TAK1/JNK signaling pathway.
Aminobutyrates
/ pharmacology
Animals
Biphenyl Compounds
/ pharmacology
Cardiotonic Agents
/ pharmacology
Caspases
/ metabolism
Cell Line
Cytokines
/ metabolism
Disease Models, Animal
Drug Combinations
Heart Injuries
/ drug therapy
Inflammasomes
/ genetics
Inflammation
/ drug therapy
Intracellular Signaling Peptides and Proteins
/ metabolism
JNK Mitogen-Activated Protein Kinases
/ genetics
MAP Kinase Kinase Kinases
/ genetics
Male
Myocardial Infarction
/ complications
Myocytes, Cardiac
/ drug effects
NLR Family, Pyrin Domain-Containing 3 Protein
/ genetics
Phosphate-Binding Proteins
/ metabolism
Pyroptosis
/ drug effects
Rats, Sprague-Dawley
Reactive Oxygen Species
/ metabolism
Signal Transduction
/ drug effects
Valsartan
/ pharmacology
LCZ696
NLRP3 inflammasome
TAK1/JNK signaling pathway
myocardial infarction
Journal
Molecular medicine reports
ISSN: 1791-3004
Titre abrégé: Mol Med Rep
Pays: Greece
ID NLM: 101475259
Informations de publication
Date de publication:
Sep 2021
Sep 2021
Historique:
received:
30
08
2020
accepted:
01
03
2021
entrez:
23
7
2021
pubmed:
24
7
2021
medline:
10
11
2021
Statut:
ppublish
Résumé
The present study aimed to investigate the protective effects of sacubitril/valsartan (LCZ696) on ventricular remodeling in myocardial infarction (MI) and the effects of the inflammasome‑mediated inflammatory response. First, a rat model was established. Animals were then treated with LCZ696 so that the histopathological changes associated with ventricular remodeling could be investigated. The serum levels of the inflammatory factors IL‑18 and IL‑1β were also determined by ELISA. Immunofluorescence was used to investigate the ratio of pyroptosis following MI modelling. Western blotting and reverse transcription‑quantitative PCR were used to detect the relative expression levels of proteins and mRNAs in the transforming growth factor β‑activated kinase‑1 (TAK1)/JNK pathway and those associated with the NLR pyrin family domain containing 3 (NLRP3) inflammasome, respectively. The present study also investigated the regulatory mechanisms and associations between the TAK1 and JNK pathways, NOD‑, leucine‑rich repeat‑ and the NLRP3 inflammasome, in H9C2 cells and myocardial cells from the rat model of MI. LCZ696 improved MI‑induced myocardial fibrosis, rescued myocardial injury and suppressed the release of inflammatory factors. With regards to myocardial cell damage, pyroptosis in cardiomyocytes was observed. The
Identifiants
pubmed: 34296299
doi: 10.3892/mmr.2021.12315
pii: 676
pmc: PMC8335743
doi:
pii:
Substances chimiques
Aminobutyrates
0
Biphenyl Compounds
0
Cardiotonic Agents
0
Cytokines
0
Drug Combinations
0
Gsdmd protein, rat
0
Inflammasomes
0
Intracellular Signaling Peptides and Proteins
0
NLR Family, Pyrin Domain-Containing 3 Protein
0
Nlrp3 protein, rat
0
Phosphate-Binding Proteins
0
Reactive Oxygen Species
0
Valsartan
80M03YXJ7I
JNK Mitogen-Activated Protein Kinases
EC 2.7.11.24
MAP Kinase Kinase Kinases
EC 2.7.11.25
MAP kinase kinase kinase 7
EC 2.7.11.25
Caspases
EC 3.4.22.-
sacubitril and valsartan sodium hydrate drug combination
WB8FT61183
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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