Necroptosis and RhoA/ROCK pathways: molecular targets of Nesfatin-1 in cardioprotection against myocardial ischemia/reperfusion injury in a rat model.
Animals
Biomarkers
/ metabolism
Cardiotonic Agents
/ therapeutic use
Disease Models, Animal
Electrocardiography
Fibrosis
Glutathione
/ metabolism
Male
Malondialdehyde
/ metabolism
Myocardial Reperfusion Injury
/ diagnostic imaging
Myocardium
/ pathology
Necroptosis
/ drug effects
Nucleobindins
/ pharmacology
Protein Serine-Threonine Kinases
/ metabolism
Rats, Wistar
Reactive Oxygen Species
/ metabolism
Receptor-Interacting Protein Serine-Threonine Kinases
/ metabolism
Signal Transduction
/ drug effects
Superoxide Dismutase
/ metabolism
rho-Associated Kinases
/ metabolism
rhoA GTP-Binding Protein
/ metabolism
Myocardial infarction
Necroptosis
Nesfatin-1
RIPK1-RIPK3-MLKL axis
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Mar 2021
Mar 2021
Historique:
received:
28
01
2021
accepted:
11
03
2021
pubmed:
24
3
2021
medline:
20
5
2021
entrez:
23
3
2021
Statut:
ppublish
Résumé
Nesfatin-1 as a new energy-regulating peptide has been known to display a pivotal role in modulation of cardiovascular functions and protection against ischemia/reperfusion injury. However, the detailed knowledge about molecular mechanisms underlying this protection has not been completely investigated yet. This study was designed to clarify the molecular mechanisms by which nesfatin-1 exert cardioprotection effects against myocardial ischemia-reperfusion (MI/R). Left anterior descending coronary artery (LAD) was ligated for 30 min to create a MI/R model in rats. MI/R rats were treated with three concentrations of nesfatin-1 (10, 15 and 20 µg/kg) then expression of necroptosis and necrosis mediators were measured by western blotting assay. Fibrosis, morphological damages, cardiac function, myocardial injury indictors and oxidative stress factors were evaluated as well. Induction of MI/R model resulted in cardiac dysfunction, oxidative stress, increased activity of RIPK1-RIPK3-MLKL axis and RhoA/ROCK pathway, extension of fibrosis and heart tissue damage. Highest tested concentration of nesfatin-1 markedly improved cardiac function. Moreover, it reduced oxidative stress, collagen deposition, and morphological damages, through inhibiting the expression of necroptosis mediators and also, necrosis including RIPK1, RIPK3, MLKL, ROCK1, and ROCK2 proteins. The lowest and middle tested concentrations of nesfatin-1 failed to exert protective effects against MI/R. These findings have shown that nesfatin-1 can exert cardioprotection against MI/R in a dose dependent manner by suppressing necroptosis via modulation of RIPK1-RIPK3-MLKL axis and RhoA/ROCK/RIP3 signaling pathway.
Identifiants
pubmed: 33755849
doi: 10.1007/s11033-021-06289-x
pii: 10.1007/s11033-021-06289-x
doi:
Substances chimiques
Biomarkers
0
Cardiotonic Agents
0
Nucb2 protein, rat
0
Nucleobindins
0
Reactive Oxygen Species
0
Malondialdehyde
4Y8F71G49Q
Superoxide Dismutase
EC 1.15.1.1
Protein Serine-Threonine Kinases
EC 2.7.11.1
RIPK1 protein, rat
EC 2.7.11.1
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ripk3 protein, rat
EC 2.7.11.1
rho-Associated Kinases
EC 2.7.11.1
rhoA GTP-Binding Protein
EC 3.6.5.2
Glutathione
GAN16C9B8O
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2507-2518Références
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