Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-kappa B/p65 Expression
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62690094%3A18470%2F18%3A50014686" target="_blank" >RIV/62690094:18470/18:50014686 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1038/s41598-018-32376-4" target="_blank" >http://dx.doi.org/10.1038/s41598-018-32376-4</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1038/s41598-018-32376-4" target="_blank" >10.1038/s41598-018-32376-4</a>
Alternative languages
Result language
angličtina
Original language name
Simvastatin Protects Cardiomyocytes Against Endotoxin-induced Apoptosis and Up-regulates Survivin/NF-kappa B/p65 Expression
Original language description
This study is aimed to investigate whether simvastatin induces cardiomyocytes survival signaling in endotoxin (lipopolysaccharide, LSP)-induced myocardial injury, and if so, further to determine a role of survivin in simvastatin-anti-apoptotic effect. Wistar rats were pretreated with simvastatin (10-40 mg/kg po) before a single non-lethal dose of LPS. In myocardial tissue, LPS induced structural disorganization of myofibrils with significant inflammatory infiltrate (cardiac damage score, CDS =3.87 +/- 0.51, p < 0.05), whereas simvastatin dose-dependently abolished structural changes induced by LPS (p < 0.01). Simvastatin in 20 mg/kg and 40 mg/kg pretreatment, dose dependently, attenuated myocardial apoptosis determined as apoptotic index (28.8 +/- 4.5% and 18.9 +/- 3.5, p < 0.05), decreased cleaved caspase-3 expression (32.1 +/- 5.8%, p < 0.01), along with significant Bcl-xL expression in the simvastatin groups (p < 0.01). Interestingly, in the simvastatin groups were determined significantly increased expression of survivin (p < 0.01), but in negative correlation with cleaved caspase-3 and apoptotic indices (p < 0.01). Simvastatin has a cardioprotective effects against LPS induced apoptosis. The effect may be mediated by up-regulation of survivin via activation of NF-kappa B, which leads to reduced activation of caspase-3 and consequent apoptosis of cardiomyocytes in experimental sepsis.
Czech name
—
Czech description
—
Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
—
OECD FORD branch
30108 - Toxicology
Result continuities
Project
—
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2018
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Scientific reports
ISSN
2045-2322
e-ISSN
—
Volume of the periodical
8
Issue of the periodical within the volume
October
Country of publishing house
GB - UNITED KINGDOM
Number of pages
10
Pages from-to
"Article Number: 14652"
UT code for WoS article
000446034000053
EID of the result in the Scopus database
2-s2.0-85054183714